Name: Oliver's mTOR Atlas
Creator: Oliver's mTOR Atlas
License: https://creativecommons.org/licenses/by/4.0/

Welcome

Ask Atlas

Pathway

Studies

Authors

Open Questions

Timeline

About

Oliver's mTOR Atlas · Welcome

Everything the landmark literature shows about mTOR — and everything it doesn’t

mTOR has plenty of maps — interaction networks, pathway diagrams, drug catalogs. Few of them make explicit how strong the evidence behind a claim actually is, or whether it has been tested in humans at all. Oliver's mTOR Atlas starts from a hand-picked corpus of landmark studies — not all of PubMed — and grades every eligible peer-reviewed primary study on an A–D evidence tier — human vs. animal, and by outcome, including the null and negative results that are easy to overlook. Ask it anything in plain language and each claim in the answer comes back cited and color-coded by evidence strength. And where the evidence runs thin, the Open Questions tab maps what is missing — and the testable hypotheses hiding inside it, each labelled so an editorial proposal is never mistaken for a finding.

—

most relevant studies

—

tested in humans

—

animal + mechanistic

1975

the story begins

The evidence pyramid

330 studies, a hundred different kinds of evidence. This shows how the Atlas's corpus is distributed across levels of evidence — from test-tube mechanisms to large human trials. Colors match the Pyramid Level tags used throughout this Atlas.

A lower rung is not a weaker paper. The pyramid ranks how directly a study can support a clinical claim about humans — it says nothing about how rigorous, original or important the science is. Several of the results this whole field rests on sit on the bottom rung: the identification of mTOR itself, the discovery of Raptor and Rictor, the cryo-EM structures of both complexes. They were published in Nature, Cell and Science and they are mechanistic. Lower evidence for clinical translation does not imply lower scientific quality. Read the pyramid as an answer to “how far is this from an outcome measured in people?”, never as a ranking of merit.

Systematic Reviewmeta-analyses

Human Clinical TrialRCTs, phase 2/3

Human Observationalnon-randomized

Animal Studymouse, fly, worm…

Mechanistic / In Vitrocells, biochemistry, structure

—

Direct human evidence

—

Animal + mechanistic

A vast knowledge base of HOW mTOR works — but only indirect evidence the same holds true in people.

Outside the evidence hierarchy

These categories describe the form a publication takes, not the strength of its evidence — which is why they sit outside the pyramid rather than inside it. They account for the remaining — studies, so the pyramid's — and these together add up to the full Atlas.

How this relates to the A–D tier. Pyramid level and evidence tier are two different axes. Every eligible peer-reviewed primary study receives an A–D tier. Narrative reviews are also peer-reviewed, so they carry the weakest tier (D) rather than no tier at all — but they sit outside the pyramid because a review is not itself an experiment. Preprints and registered trials receive no A–D tier in either direction: a preprint has not been reviewed, and a registered trial has no results yet, so grading them would invent a strength that does not exist. They are labelled as what they are.

Narrative Review—

Preprint (not peer-reviewed)—

Registered Trial (ongoing)—

Oliver's mTOR Atlas · Open Questions

Where the evidence runs out.

What we don’t know — and why

How to read these, and how not to. Gaps here are computed against this corpus, not against the literature. A gap means the Atlas holds no linking study — which may mean none exists, or may mean the corpus is incomplete. That distinction is not cosmetic: gap H1 originally claimed the amino-acid sensors link to zero ageing outcomes, and an external review found a 2010 Science paper that did exactly that. It has since been added and the gap narrowed. Treat every gap below as a hypothesis about the evidence, testable by finding the paper that closes it.

A pathway map shows what is known. This section is the opposite: gaps surfaced automatically by joining the Atlas’s entity graph to each study’s evidence tier (A>B>C>D). Two structural findings, then 10 testable hypotheses — each anchored to the studies that define the gap. Click any study code to open it.

Every block below is labelled by what kind of claim it is

Established What the corpus actually contains: published, peer-reviewed results and the tier structure over them. Checkable against the cited studies.

Interpretation A reading of what those results mean together. The underlying findings are solid; the joining-up is a judgement, and other readings are possible.

Editorial hypothesis Not established by anyone. A proposal generated by this Atlas about what might be true and how it could be tested. Nothing carrying this label has been demonstrated. Do not cite it as a finding. The confidence number on each card is the curator’s subjective prior that the hypothesis is worth testing — not a probability that it is true, and not a statistic.

InterpretationNutrient-sensor evidence desert

Every amino-acid sensor and upstream regulator (Sestrin2, CASTOR1, SAMTOR, Rag GTPases, GATOR1/2, Ragulator, Rheb, PRAS40, AMPK) rests only on tier-D mechanistic evidence - and the sensors link to ZERO longevity / aging outcomes. The most drug-specific part of the pathway is phenotype-untested.

InterpretationHuman hard-endpoint desert

Of 32 longevity-linked studies, 20 are tier-C animal; the four human entries are safety, immune or observational - none with a lifespan or healthspan primary endpoint. The one trial that could deliver it (EVERLAST) has no results yet.

H1Sensor-selective geroprotection without the metabolic penaltyEvidence desertconfidence 0.75

EstablishedWhy it is a gap (evidence basis)

Every amino-acid sensor (Sestrin2, CASTOR1, SAMTOR, v-ATPase) is supported ONLY by tier-D mechanistic studies and links to ZERO aging/longevity outcomes. They are the most pharmacologically specific nodes yet phenotype-untested.

Editorial hypothesisWhat might be true

Dialing down mTORC1 through ONE sensor arm (e.g. methionine restriction via SAMTOR->GATOR1, or leucine via Sestrin2) reproduces rapamycin's healthspan benefit while sparing mTORC2 - and therefore without insulin resistance.

Not established by anyone. This is a proposal generated by this Atlas — do not cite it as a finding.

Editorial hypothesisProposed experiment — not yet run

Mouse: (i) SAMTOR gain-of-function / dietary methionine restriction, (ii) rapamycin, (iii) control. Endpoints: healthspan/lifespan, glucose tolerance, mTORC2 activity (Akt-Ser473). Prediction: (i) matches (ii) on healthspan but not on glucose impairment.

Supporting studies

GU2017SAX2015LAM2012

H2mTORC1-selective (mTORC2-sparing) dosing captures longevity without insulin resistanceContradiction / tensionconfidence 0.85

EstablishedWhy it is a gap (evidence basis)

Longevity comes from mTORC1 but chronic rapamycin's harm (insulin resistance) comes from mTORC2 disruption (LAM2012). QUANTIFIED (full text): ARR2015 - daily 2 mg/kg rapamycin impaired glucose tolerance (+71% AUC) and inhibited BOTH mTORC1 and mTORC2 (AKT-S473), while weekly / every-5-days caused NO glucose impairment and inhibited mTORC1 only -> intermittent dosing decouples benefit from harm in vivo. Dose-response MIL2014 (4.7/14/42 ppm; top dose +23% M / +26% F). PEARL tested 5 vs 10 mg/week but its primary endpoint was visceral fat (missed) - no mTORC1-selective human aging readout exists. UPDATE (2026-07-09, revised 2026-07-29): early clinical evidence now exists outside the rapamycin/rapalog class. Bi-steric mTORC1-selective inhibitors (>25-fold selectivity over mTORC2) were validated preclinically (MEN2023: RMC-6272 overcomes drug resistance via complete mTORC1 suppression, sparing mTORC2) and clinically (SCH2025: RMC-5552 Phase 1, n=57 solid tumors) -- treatment-related hyperglycemia was only 4%, which is consistent with the hypothesis that sparing mTORC2 reduces the glucose-intolerance signature seen with chronic rapamycin/rapalogs. Because SCH2025 was open-label, single-arm and had no rapamycin or ATP-site comparator, the low hyperglycaemia rate is a supportive signal, not a causal attribution: it is compared against historical rapalog experience, not against a randomised control. This is the strongest human evidence yet for the mechanistic premise of H2, but it is preliminary, and it comes from an oncology trial, not an aging/longevity endpoint -- the missing link is still a healthspan/lifespan readout for a selective inhibitor.

Editorial hypothesisWhat might be true

An intervention that suppresses the mTORC1/4E-BP1 arm while sparing mTORC2 -- now achievable with bi-steric mTORC1-selective inhibitors (RMC-6272/RMC-5552) in addition to intermittent/low-dose rapamycin -- yields the lifespan benefit without glucose intolerance.

Not established by anyone. This is a proposal generated by this Atlas — do not cite it as a finding.

Editorial hypothesisProposed experiment — not yet run

Mouse lifespan under continuous vs intermittent vs low-dose rapamycin; endpoints lifespan + insulin sensitivity + mTORC2 activity (Akt-Ser473). Mirrors the human EVERLAST daily-vs-weekly design. NEW (sharper test enabled by 2023-2025 tools): repeat using a bi-steric mTORC1-selective inhibitor (RMC-6272 class) instead of rapamycin -- this removes the mTORC2-sparing question as a confound, so if lifespan extension still occurs without glucose intolerance, that is a cleaner causal test than intermittent-dosing rapamycin.

Supporting studies

LAM2012ARR2015MIL2014KEN2016THO2009MOE2025NCT0583MEN2023SCH2025

H3Muscle-sparing, pulsed mTORC1 inhibitionContradiction / tensionconfidence 0.70

EstablishedWhy it is a gap (evidence basis)

mTORC1 is required for muscle (raptor-KO dystrophy; DRU2009 blocks human MPS; ROM2001 hypertrophy) yet mTOR inhibition is the leading longevity lever. QUANTIFIED: BIT2016 transient rapamycin (8 mg/kg i.p. x 90 days) -> males +60% post-treatment life expectancy (p=0.02), but females NO survival benefit (p=0.26) and MORE aggressive hematopoietic cancers (16/16 vs 6/12 controls, p=0.002). So 'transient dosing captures the benefit' holds, but sex-specifically and with a female harm signal a pulsed/muscle-sparing design must control for.

Editorial hypothesisWhat might be true

Time-restricted / pulsed mTORC1 inhibition (drug trough permitting post-exercise anabolic windows) preserves muscle mass while still capturing the longevity benefit.

Not established by anyone. This is a proposal generated by this Atlas — do not cite it as a finding.

Editorial hypothesisProposed experiment — not yet run

Mouse: continuous vs pulsed rapamycin timed around resistance loading; endpoints lifespan + muscle mass/fiber CSA + autophagic flux (LC3-II/p62). Prediction: pulsed arm preserves muscle at similar healthspan.

Supporting studies

DRU2009ROM2001MOE2025BIT2016

H4Is autophagy actually REQUIRED for the mammalian lifespan benefit?Mechanism-to-outcome gapconfidence 0.70

EstablishedWhy it is a gap (evidence basis)

Autophagy is assumed to mediate longevity but shown directly only in fly/worm (BJE2010, MEL2003) and by Atg5 overexpression in mouse (PYO2013). No study tests whether BLOCKING autophagy abolishes rapamycin's mammalian lifespan extension.

Editorial hypothesisWhat might be true

Autophagy is necessary: rapamycin will FAIL to extend lifespan in autophagy-deficient (e.g. inducible Atg7-KO) mice.

Not established by anyone. This is a proposal generated by this Atlas — do not cite it as a finding.

Editorial hypothesisProposed experiment — not yet run

Rapamycin x inducible tissue-wide autophagy-KO mouse lifespan study, with a wild-type rapamycin arm as positive control.

Supporting studies

BJE2010MEL2003PYO2013

H5A sensor/autophagy biomarker panel as a surrogate endpoint for human trialsHuman-endpoint gapconfidence 0.70

EstablishedWhy it is a gap (evidence basis)

QUANTIFIED human-endpoint desert: EVERY completed human trial with an aging/healthspan PRIMARY endpoint missed it or was safety-only. PEARL (MOE2025): visceral fat NOT met (secondary bone density OR 0.24, 95% CI 0.06-0.93, p=0.04). RTB101 phase 3 (MAN2021): symptomatic-RTI primary NOT met. Resveratrol (POU2013): fully negative. CALERIE (ROM2016): safety only, no significant differences. The human 'wins' are disease indications (BOLERO-2, RADIANT-3 PFS 5% vs 2%) or surrogate biomarkers (topical rapamycin epidermal p16 reduced, p=0.008). Not 'few trials' but ZERO with a hard aging endpoint. UPDATE (2026-07-09): a candidate real-time readout tool for the mTORC1-vs-mTORC2 arm of the panel now exists -- AIMTOR (BOU2020), a genetically encoded BRET biosensor validated in human and mouse cells that reads mTOR activity live, including subcellular resolution (lysosome/cytosol/nucleus/mitochondria). This does not fill the human-endpoint desert itself, but it derisks the panel's feasibility: the biosensor arm is no longer a proposed capability, it is a published, working assay.

Editorial hypothesisWhat might be true

A pathway-activity panel (SAMTOR/GATOR readout + LC3-II/p62 autophagic flux + mTORC1-vs-mTORC2 substrate phosphorylation) tracks lifespan-extending interventions and can serve as a validated surrogate, enabling short human geroprotection trials.

Not established by anyone. This is a proposal generated by this Atlas — do not cite it as a finding.

Editorial hypothesisProposed experiment — not yet run

Back-test the panel across the animal longevity studies in the corpus (does it separate lifespan-extending from null interventions?), then validate prospectively against EVERLAST's daily-vs-weekly arms. The mTORC1-vs-mTORC2 substrate-phosphorylation arm can now build directly on AIMTOR (BOU2020) rather than needing de novo assay development.

Supporting studies

MOE2025MAN2021POU2013ROM2016CHU2019BAS2012YAO2011LEE2024NCT0583BOU2020

H6Sex dimorphism in mTOR-longevity responses is pervasive and sometimes direction-flippingContradiction / tensionconfidence 0.80

EstablishedWhy it is a gap (evidence basis)

Emerged directly from the full-text effect sizes: S6K1-KO +19% median lifespan in FEMALES / no effect in males (SEL2009); rapamycin favors females (MIL2014 all doses in F vs top-2 in M; HAR2009 +38% F vs +28% M; FOK2014 +16% F vs +11% M; WUX2013 +22% F/+19% M; BIT2016 male benefit but female harm); yet acarbose favors MALES (+22% vs +5%, HAR2014). Sex changes not just the magnitude but sometimes the DIRECTION of the response.

Editorial hypothesisWhat might be true

Sex-specific pharmacokinetics (females reach higher rapamycin blood levels, MIL2014) plus pharmacodynamic differences drive the dimorphism; matching blood exposure across sexes will narrow the gap for rapamycin, but not for interventions with the opposite skew (acarbose), which must be target-driven.

Not established by anyone. This is a proposal generated by this Atlas — do not cite it as a finding.

Editorial hypothesisProposed experiment — not yet run

Sex-stratified, dose-matched study: titrate rapamycin to equal blood levels in males and females; measure lifespan/healthspan + mTORC1 vs mTORC2 signaling, separating PK (exposure) from PD (tissue response). Repeat for acarbose to test whether its male-skew is exposure- or target-driven.

Supporting studies

SEL2009MIL2014HAR2009FOK2014WUX2013BIT2016HAR2014

H7Low-dose mTOR inhibition rejuvenates the aging immune system without net immunosuppressionContradiction / tensionconfidence 0.75

EstablishedWhy it is a gap (evidence basis)

mTOR inhibition is the textbook immunosuppressant (HEI1991: rapamycin arrests the cell cycle; used clinically against transplant rejection), yet the SAME pathway at LOW dose is one of the few mTOR interventions with POSITIVE human data. QUANTIFIED: MAN2014 - 6 weeks low-dose RAD001 (everolimus) in elderly IMPROVED influenza-vaccine antibody titers (~20% rise vs placebo) and reduced exhausted PD-1+ CD4/CD8 T cells. MAN2018 - the RTB101 +/- everolimus 2a/2b program cut lab-confirmed respiratory tract infections and upregulated interferon-induced antiviral genes; only the 10 mg/day RTB101 dose worked. But MAN2021 (phase 3 PROTECTOR-1) MISSED its primary endpoint (clinically symptomatic respiratory illness NOT reduced) - so the human immune 'win' collapsed at scale. Mechanistic anchors show the pathway cuts both ways: ARA2009 mTOR drives memory-CD8 differentiation and ZEN2013 mTORC1 is REQUIRED for Treg function, so over-inhibition would blunt immunity; LV2026 shows age-related Lamtor5 loss itself drives immunosenescence. The unresolved tension: the dose that rejuvenates adaptive immunity and the dose that suppresses it are not separated, and no human trial has hit a durable clinical immune endpoint.

Editorial hypothesisWhat might be true

There is a narrow low-dose / intermittent window in which mTORC1 inhibition reverses T-cell exhaustion and boosts vaccine and antiviral responses in the elderly while leaving protective Treg/effector immunity intact - i.e. net immune REJUVENATION, not suppression. Above that window the effect flips to classical immunosuppression. The phase 3 failure reflects a dose/endpoint mismatch, not absence of the effect.

Not established by anyone. This is a proposal generated by this Atlas — do not cite it as a finding.

Editorial hypothesisProposed experiment — not yet run

Dose-ranging elderly RCT with a validated immune-function primary endpoint (T-cell exhaustion markers + neoantigen/vaccine seroconversion + lab-confirmed infection incidence), testing several low/intermittent rapalog schedules against placebo, with paired PBMC mTORC1 vs mTORC2 phosphosignatures to map the rejuvenation-vs-suppression crossover. Prediction: an inverted-U where mid-low doses maximize vaccine response and minimize infections, with immunosuppression only above a definable trough.

Supporting studies

MAN2014MAN2018MAN2021HEI1991ARA2009ZEN2013LV2026LEE2024

H8Brain-penetrant mTOR inhibition clears neurodegenerative aggregates in models but has zero human cognitive-aging endpoint - and mTORC2 is needed for memoryMechanism-to-outcome gapconfidence 0.70

EstablishedWhy it is a gap (evidence basis)

The preclinical CNS case for mTOR inhibition is unusually deep, yet every outcome is in animals/models and the mTORC2 arm creates a built-in liability. Aggregate-clearance evidence: SPI2010 rapamycin lowered amyloid-beta and abolished cognitive deficits in an AD mouse model (autophagy-dependent); ZHO2009 mTORC1 inhibition suppressed anatomical/behavioral abnormalities; CAC2010 mapped the mTOR-amyloid-tau triangle onto cognition; TAN2024 (preprint) restored tau-induced metabolic, mitochondrial and cognitive deficits; EHN2008 reversed learning deficits in Tsc2+/- mice. BUT the same drug carries a cognitive downside signal: HAL2012 found chronic rapamycin modulates BOTH cognitive AND non-cognitive (anxiety-like) behavior, and mTORC2 supports dendritic protein synthesis, synaptic plasticity and long-term memory consolidation - the arm chronic rapamycin also disrupts. Net: strong tier-C/D mechanism, ZERO tier-A/B human neurodegeneration or cognitive-aging outcome, and an unquantified trade-off between clearing aggregates (mTORC1/autophagy) and preserving plasticity (mTORC2).

Editorial hypothesisWhat might be true

An intermittent or mTORC1-selective, CNS-penetrant regimen enhances autophagic clearance of amyloid/tau/alpha-synuclein enough to slow cognitive decline in early neurodegeneration WITHOUT the mTORC2-dependent memory/plasticity penalty seen with chronic pan-mTOR inhibition. The healthspan-relevant readout (delayed cognitive decline) is therefore achievable but has never been tested in humans.

Not established by anyone. This is a proposal generated by this Atlas — do not cite it as a finding.

Editorial hypothesisProposed experiment — not yet run

Two-step: (i) mouse tauopathy/amyloid models comparing chronic pan-rapamycin vs intermittent vs mTORC1-selective (bi-steric) dosing - endpoints aggregate load, autophagic flux (LC3-II/p62), hippocampal LTP, and Morris-water-maze memory, to isolate the mTORC2/plasticity cost. (ii) A biomarker-anchored early-AD human pilot (CSF/plasma p-tau and amyloid PET as surrogate) on the winning schedule. Prediction: intermittent/selective arms clear aggregates with preserved LTP and memory; chronic pan-inhibition clears aggregates but degrades plasticity.

Supporting studies

SPI2010ZHO2009CAC2010HAL2012EHN2008TAN2024LAM2012LEE2024

H9Rapamycin + AMPK-axis drugs (acarbose / metformin): additive via distinct pathways, and untested as a combination in humansEvidence desertconfidence 0.70

EstablishedWhy it is a gap (evidence basis)

Animal combination data are suggestive but the human evidence for combining mTOR inhibition with AMPK-axis geroprotectors is a desert. QUANTIFIED (ITP): rapamycin + acarbose from 9 months extended MALE lifespan MORE than either drug alone, while in FEMALES the combination was no better than rapamycin alone - consistent with acarbose acting through a largely mTOR-INDEPENDENT (postprandial-glucose) route and hence adding rather than overlapping. HAR2014 established acarbose's male-skewed lifespan effect. The AMPK arm converges back onto mTOR mechanistically: ZHO2001 metformin acts via AMPK, GWI2008 AMPK phosphorylates raptor to gate mTORC1, HOW2017 metformin inhibits hepatic mTORC1 dose-dependently via AMPK - which raises the opposite possibility that metformin + rapamycin are partly REDUNDANT on the mTORC1 node. Human signal exists only for monotherapy-ish observation (BAN2014: type-2 diabetics on metformin outlived non-diabetic controls). No study - animal or human - cleanly separates ADDITIVE (distinct pathways) from REDUNDANT (same node) for these pairs, and there is no human combination trial at all.

Editorial hypothesisWhat might be true

Rapamycin combined with a glucose-route geroprotector (acarbose) is ADDITIVE because the second drug works largely outside mTOR, whereas rapamycin combined with an AMPK-mTORC1 drug (metformin) is largely REDUNDANT on the mTORC1 node and yields sub-additive lifespan/healthspan gains. Metformin's main value alongside rapamycin is not additive longevity but mitigation of rapamycin's glucose intolerance.

Not established by anyone. This is a proposal generated by this Atlas — do not cite it as a finding.

Editorial hypothesisProposed experiment — not yet run

Factorial mouse lifespan/healthspan study (vehicle / rapamycin / acarbose / metformin / rapamycin+acarbose / rapamycin+metformin), sex-stratified, with mTORC1 (S6K/4E-BP1) and AMPK (raptor-Ser792) readouts plus glucose tolerance. Test for statistical super-additivity. Prediction: rapamycin+acarbose is additive on lifespan; rapamycin+metformin is sub-additive on lifespan but restores glucose tolerance. Follow with a human factorial healthspan-biomarker trial on the additive pair.

Supporting studies

HAR2014ZHO2001GWI2008HOW2017BAN2014ARR2015MOE2025

H10Suppression of senescence/SASP (geroconversion), not just autophagy, is the mediator of rapamycin's healthspan benefitMechanism-to-outcome gapconfidence 0.70

EstablishedWhy it is a gap (evidence basis)

H4 asks whether autophagy is REQUIRED for the lifespan benefit; this gap proposes a parallel, partly autophagy-INDEPENDENT mediator that is equally untested at the outcome level. Evidence that mTOR gates senescence: DEM2009 rapamycin decelerates cellular senescence (geroconversion from arrest to senescence); BLA2006 framed aging as quasi-programmed mTOR-driven cellular hyperfunction pharmacologically inhibitable by rapamycin; LAB2015 mTOR directly regulates the pro-tumorigenic SASP (via MK2/ZFP36L1 control of secreted-factor mRNAs); CAS2009 mTOR drives Wnt-induced epidermal stem-cell exhaustion; LV2026 links Lamtor5-mTOR to cGAS-driven immunosenescence. Crucially, external work shows rapamycin still suppresses SASP in Nrf2-KO fibroblasts WITHOUT activating autophagy - i.e. SASP suppression can be autophagy-independent. Human anchor: CHU2019 topical rapamycin REDUCED senescence markers (p16INK4a) in human skin (p=0.008) - the rare direct human PD readout, but on skin, not a systemic aging endpoint. Missing: no study tests whether BLOCKING senescence suppression (or clearing senescent cells independently) reproduces or abolishes rapamycin's mammalian healthspan gain, so autophagy vs geroconversion as the dominant mediator is unresolved.

Editorial hypothesisWhat might be true

Rapamycin's healthspan benefit is mediated substantially by suppressing mTOR-driven geroconversion and the SASP - not solely by inducing autophagy. Therefore rapamycin's benefit will persist in autophagy-deficient tissue as long as senescence/SASP suppression is intact, and will be largely OCCLUDED by a senolytic (removing the target senescent-cell burden leaves rapamycin little to suppress).

Not established by anyone. This is a proposal generated by this Atlas — do not cite it as a finding.

Editorial hypothesisProposed experiment — not yet run

Two crossed tests in mice: (i) rapamycin in an inducible autophagy-KO (shared with H4's design) with senescence/SASP burden (p16, IL-6, SA-beta-gal) as the readout - does rapamycin still cut SASP and preserve healthspan without autophagy? (ii) Rapamycin +/- a senolytic (e.g. dasatinib+quercetin): epistasis test - if benefits are non-additive/occluded, senescence suppression is the shared mechanism; if additive, they are parallel. Endpoints: healthspan/frailty index, tissue senescence load, lifespan.

Supporting studies

DEM2009BLA2006LAB2015CAS2009LV2026CHU2019PYO2013

Oliver's mTOR Atlas · Timeline

How mTOR biology actually grew

Every node is a landmark study. Every edge is a claim about what one study made possible for the next. The vertical axis is real time, so the empty stretches are part of the argument. Nodes carry the Atlas's own evidence tiers: blue is direct human evidence. Count the blue.

This is an editorial reconstruction, not a citation network. Nothing on this canvas is computed from citation data, co-citation, or any bibliometric measure. Each edge is a judgement made by the curator — “study A is what made study B askable” — written down so it can be argued with. Two researchers reading the same papers could reasonably draw a different tree, and the absence of an edge is not evidence that no influence existed. Treat the shape as an interpretation of how the field moved, and the nodes and their metadata (PubMed-verified) as the checkable part.

Drag to pan · scroll/pinch or +/− to zoom

Study metadata retrieved and verified via PubMed; evidence tiers follow the Atlas's own A–D scheme. Lineage edges are an editorial reconstruction — they encode enablement, extension, convergence, contradiction and open questions as judged by the curator, and are not derived from citation counts, co-citation, or any other bibliometric signal. They are a claim about influence, offered to be challenged. Node positions, edges, counts and the translation gap are computed at runtime from the LINEAGE array; nothing is hardcoded. Add a study and the tree grows.

How we got here

Every entry in this Atlas traces back to a real paper. Here are six moments that built the field — from a soil sample on a Pacific island to a large clinical trial that missed its primary endpoint. These six are a curator's selection, not a consensus list.

1975

A molecule from Rapa Nui

Vézina and colleagues isolate a compound from Streptomyces bacteria in a soil sample from Rapa Nui (Easter Island), with antifungal activity nobody can yet explain. They name it after the island: rapamycin. DOI: 10.7164/antibiotics.28.721

1994

The target gets a name

Sabatini and colleagues identify the protein rapamycin actually binds inside human cells — the Mammalian Target Of Rapamycin. Two decades of "what does this drug even do?" finally has a molecular answer. DOI: 10.1016/0092-8674(94)90570-3

2002–2004

One protein, two complexes

Kim et al. discover Raptor, the partner protein that defines mTOR Complex 1. Two years later, Sarbassov et al. discover Rictor — defining a second, rapamycin-resistant complex, mTORC2. mTOR turns out to have two faces at the molecular level too. DOI: 10.1016/s0092-8674(02)00808-5 · DOI: 10.1016/j.cub.2004.06.054

2009

The first drug shown to extend mammalian lifespan

The NIA Interventions Testing Program, led by Harrison and colleagues, shows rapamycin extends lifespan in genetically heterogeneous mice — even when treatment starts late in life. First pharmacological intervention ever shown to do this in a mammal. DOI: 10.1038/nature08221

2018

From mice to people

Mannick and colleagues show low-dose mTOR inhibition reduces infection rates and improves vaccine response in elderly volunteers — the first hint the mouse result might translate to humans. DOI: 10.1126/scitranslmed.aaq1564

2021

The reality check

The follow-up phase 3 trial — 1,024 participants — misses its primary endpoint. The drug still switched on the right antiviral genes; it just didn't reduce clinically symptomatic illness. This Atlas keeps that result next to the success that came before it, because a database that only remembers the wins isn't science. DOI: 10.1016/S2666-7568(21)00062-3

Oliver's mTOR Atlas · About

The person and the project.

What this project is

Oliver's mTOR Atlas is an evidence-graded, literature-grounded platform for the mTOR signaling pathway — not just a record of what's known, but a tool for asking how strongly it's known. You can query it in plain language — Ask Atlas returns the relevant studies ranked, tiered, and cited, with each claim color-coded by the strength of the evidence behind it — and it actively surfaces where the corpus runs out, in the Open Questions tab, turning those gaps into labelled, testable hypotheses.

It currently holds 120 cross-linked entities and 330 studies, spanning:

Upstream regulators — PI3K, Akt, TSC1/TSC2, Rheb, the Rag GTPases, Sestrin2, AMPK, and the growth hormone/IGF-1 axis further upstream still
Two core complexes — mTORC1 and mTORC2 — and their direct downstream effectors: S6K1, ULK1, Atg5
Drugs, supplements, and interventions — rapamycin, everolimus, temsirolimus, metformin, acarbose, caloric restriction, macronutrient ratio, leucine/BCAA restriction — alongside supplements like resveratrol and curcumin that were tested and did not extend lifespan under the conditions tested
Outcomes and disease contexts — longevity, autophagy, muscle growth, immune function, kidney transplant rejection, renal cell carcinoma, Huntington's disease, Alzheimer's disease — plus side effects, like the insulin resistance that comes with chronic rapamycin dosing

Every entry traces back to a specific paper, indexed with its evidence grade (an A–D tier where the study is an eligible peer-reviewed primary study, otherwise an out-of-hierarchy label), model organism, and DOI.

How the A–D tier is actually decided. The tier tracks what kind of claim a study can support, not simply which organism it used. A whole-organism study whose purpose is an organismal phenotype — lifespan, degeneration, glucose tolerance — is graded C. A whole-organism study whose purpose is signalling mechanism is graded D. This is why the fruit-fly papers split: lifespan and degeneration studies sit at C, while signalling-epistasis studies sit at D, and yeast splits the same way. The reason is deliberate: evidence strength for a health claim should follow the claim, not the taxon.

This was applied consistently but never written down until an external review in July 2026 pointed out that the stated definition ("C = animal in vivo") did not match the practice, which made the grading look arbitrary from outside. Two records were genuinely wrong and have been corrected: one carried a C tier with an in-vitro pyramid level in the same record, and one whole-mouse metabolic study was graded as in-vitro mechanism. A validator rule (R7) now blocks any deploy where the tier and the pyramid level disagree.

It deliberately includes negative results — studies where a popular longevity compound did not extend lifespan — because a database that only shows positive findings misrepresents the actual state of the science. The Interventions Testing Program's published null results for resveratrol, curcumin, and simvastatin sit in the Atlas with the same visibility as the positive rapamycin findings.

What makes it different

Pathway databases like Reactome or KEGG map the biochemistry. PubMed lets you search papers one at a time. General AI research tools read across the whole of PubMed, but in our testing they rarely make the weight of a mouse study versus a human trial explicit in the answer. To our knowledge, few resources combine these three things — though the Atlas has not surveyed every tool in the field, and if one already does, it should be used instead:

Narrow, hand-curated corpus — landmark mTOR studies, deep and low-noise rather than broad and shallow
Explicit evidence grade on every claim — an A–D tier for every eligible peer-reviewed primary study, and an explicit out-of-hierarchy label (preprint, narrative review, registered trial) for the rest, so an answer visibly separates what rests on a human RCT from what rests on a cell-culture experiment or an ungraded preprint
An Open Questions layer — points to where the evidence is thin, contradictory, or missing entirely, and reframes those gaps as testable hypotheses, with every block labelled established, interpretation or editorial hypothesis so a proposal is never read as a result

So you can ask "what's the actual evidence, at what tier, that rapamycin extends lifespan in humans and not just mice?" and get a direct answer with the receipts attached — and, just as important, an explicit map of what the Atlas's corpus does not establish.

Built narrow, starting with mTOR, by someone still early enough in their scientific training to insist that every claim traces back to a real paper.

How it's built and kept current

Every study enters the Atlas through the same four-step pipeline:

1. Source

Candidate papers are found via PubMed, prioritizing landmark discovery papers, systematic reviews, and large human RCTs over secondary commentary.

2. Verify

Each citation's PMID, DOI, year, and journal are confirmed against PubMed metadata before the entry is written — no citation is added from memory alone.

3. Grade

Every study gets an evidence tier (A = systematic review of human data, down through animal, invertebrate, and mechanistic-only) based on the strength of the model system, not the size of the headline finding.

4. Link

Entities mentioned in the study (genes, drugs, outcomes) are connected to it in the graph, so the same paper surfaces wherever any of its subjects is explored.

Every entity and study in the Atlas is sourced from primary, checkable resources — never from secondary write-ups or memory.

PubMed

The NIH's biomedical literature index. Primary source for study metadata — title, authors, journal, date, and DOI are pulled and verified against PubMed's own record before an entry is written.

bioRxiv

Source for preprints — studies not yet peer-reviewed. These are explicitly flagged as preprints, never treated as equivalent to published work.

ClinicalTrials.gov

U.S. registry of clinical trials. Lets the Atlas show ongoing human studies and what they're testing, even before results exist.

Publisher DOIs

Every DOI resolves to the publisher's own page — Nature, Cell, Science, NEJM, Lancet, and others — so any claim traces back to the original paper in one click.

Editorial policy — how studies are chosen

The most reasonable question to ask a curated database is: why these papers and not others? This section answers that, including where the answer is unsatisfying.

Why a corpus of this size at all. A PubMed query for "mTOR" returns on the order of sixty thousand records. The Atlas is not trying to be a complete index of that literature — PubMed already is one, and it is better at it. The Atlas is trying to be small enough that every single entry can be read, graded and defended by a human, and connected to the pathway by hand. The corpus size (currently 283) is therefore a consequence of that constraint, not a target: it is roughly the number of papers one person can hold to this standard. It will grow slowly and deliberately.

Inclusion criteria. A study earns a place only if it does at least one of four things —

establishes a landmark mechanism in mTOR biology
supplies the strongest available human evidence for a claim (a systematic review or a large RCT, not an isolated small trial)
fills in representative animal or mechanistic work for a pathway node that would otherwise be uncovered
reports a negative or null result that the rest of the literature tends to under-report

That last category is deliberate — the Interventions Testing Program's null findings for resveratrol, curcumin, and simvastatin are included with the same visibility as the positive rapamycin results, because a database that only shows what worked misrepresents the actual state of the science.

Exclusion criteria. A candidate is left out if it is a secondary commentary, editorial or news piece rather than a primary study or review; if it duplicates a pathway node already covered by a stronger study, and adds no new claim; if its metadata cannot be verified against PubMed (no PMID or DOI resolvable to the publisher's own record); or if its connection to mTOR is incidental — mTOR measured as one readout among many in a paper about something else. Preprints and registered trials are admitted only when they are the best available evidence for a claim, and are then labelled as ungraded rather than given an A–D tier.

How many were excluded — an honest gap. The Atlas does not currently keep a screening log. Candidates that were considered and rejected leave no record, so no exclusion count can be quoted, and none should be inferred. That is a real weakness compared with a systematic review, where the screening flow is the evidence that the search was unbiased. Here it is not: selection is a judgement call, made paper by paper, and it is not currently auditable from the outside. Anyone using the Atlas should read it as a curated reading list with grades attached, not as a systematic review of the mTOR literature. Logging rejected candidates and their reason is a planned change.

Who reviews the selection. One person: the curator. There is no second reviewer, no editorial board, and no independent adjudication of borderline calls — the usual safeguard against a single reader's blind spots is absent. The one external check to date was an unsolicited scientific review in July 2026, which produced sixteen findings; these were addressed rather than quietly dropped, and one of them exposed a real inconsistency between the stated A–D definition and the applied one (documented above, with a validator rule now blocking the class of error).

How often it updates. An automated job screens PubMed for new candidate mTOR studies and relevant conferences once daily, at 02:00, and flags anything worth adding; the decision to include and grade a flagged paper is made by hand, and publishing the updated site is a manual step. So the screening is daily, but the corpus changes only when a human accepts a candidate — typically a handful of papers a month, sometimes none. The exact timestamp of the live corpus is printed in the footer of every page, and every count on this site is computed from that snapshot rather than typed in.

Every candidate that survives the criteria is run through the four-step pipeline above (Source → Verify → Grade → Link) before it's added. So "relevant" is a curation judgment made once, up front, against explicit criteria — not a search-time popularity ranking, and not simply everything PubMed returns for "mTOR."

Author

Oliver Barton

Creator & Curator — Prague, Czech Republic — Age 15

I am a high school student in Prague with a self-directed research interest in mTOR signaling, longevity biology, and evidence-based science curation. I started Oliver's mTOR Atlas to build the kind of resource I wished existed when I began reading primary literature on the pathway: one structured database that holds studies, mechanisms, interventions, and honest evidence grades side by side, rather than scattered across dozens of review articles and pathway maps.

My current focus is mTOR regulation under dynamic rather than steady-state conditions — most of the literature treats mTORC1/mTORC2 activity as fixed rather than something that shifts over time in a real cell. I am interested in whether the pattern of activity over time — not just its average level — is what actually shapes outcomes like autophagy or growth, one of the open questions raised in this Atlas's Open Questions tab.

Contact — oliver.barton1113(at)gmail.com

Related studies — Oliver's current focus

The foundational and most closely related studies behind the “pattern over time, not just average level” question above, ranked by scientific significance rather than publication date:

Study	Authors	Why it matters	Tier
Tuberous sclerosis complex gene products, Tuberin and Hamartin, control mTOR signaling by acting as a GTPase-activating protein complex toward Rheb TEE2003 · DOI: 10.1016/s0960-9822(03)00506-2	Tee AR; Cantley LC et al. (2003)	Founding paper — first to show TSC1/TSC2 acting as the GAP complex for Rheb, the discovery the whole TSC→mTORC1 axis rests on.	D
Rheb GTPase is a direct target of TSC2 GAP activity and regulates mTOR signaling INOK2003 · DOI: 10.1101/gad.1110003	Inoki K; Guan KL et al. (2003)	Companion founding paper, published independently and simultaneously with Tee et al. 2003 — same weight, same discovery.	D
TSC2 is phosphorylated and inhibited by Akt and suppresses mTOR signalling INO2002 · DOI: 10.1038/ncb839	Inoki K; Guan KL et al. (2002)	Established the Akt→TSC2→mTOR link — the exact “known regulatory input” Joshi 2024 shows is bypassed during interphase.	D
TBC1D7 is a third subunit of the TSC1-TSC2 complex upstream of mTORC1 DIB2012 · DOI: 10.1016/j.molcel.2012.06.009	Dibble CC; Manning BD et al. (2012)	Completed the parts list of the TSC complex whose GAP activity Joshi 2024 studies across the cell cycle.	D
Spatial control of the TSC complex integrates insulin and nutrient regulation of mTORC1 at the lysosome MEN2014 · DOI: 10.1016/j.cell.2013.11.049	Menon S; Manning BD et al. (2014)	Closest mechanistic precedent to the “timing, not just level” question — shows TSC complex localization, not just abundance, gates mTORC1.	D
Molecular logic of mTORC1 signalling as a metabolic rheostat VAL2019 · DOI: 10.1038/s42255-019-0038-7	Valvezan AJ; Manning BD et al. (2019)	Conceptual framework from Joshi 2024's own senior author — mTORC1 as a graded rheostat rather than an on/off switch.	D
mTORC1 Couples Nucleotide Synthesis to Nucleotide Demand Resulting in a Targetable Metabolic Vulnerability VAL2017 · DOI: 10.1016/j.ccell.2017.09.013	Valvezan AJ; Manning BD et al. (2017)	Same lab's translational angle — TSC-mutant cells' nucleotide synthesis as a druggable weak point.	D
mTORC1 activity oscillates throughout the cell cycle, promoting mitotic entry and differentially influencing autophagy induction JOS2024 · DOI: 10.1016/j.celrep.2024.114543	Joshi JN; Valvezan AJ et al. (2024)	The paper that sparked this focus — mTORC1 activity is lowest in mitosis/G1 and highest in S/G2, and this timing, not just average level, shapes autophagy sensitivity.	D
Inferring feedback regulation from static snapshots of a single signal GIN2026 · DOI: 10.1016/j.bbrep.2026.102747	Ginzberg M; Kafri R et al. (2026)	A method for reading a signal’s change over time out of still images — and it finds AKT feedback that exists only in a narrow window at G1/S, which the authors attribute to mTORC1/S6K1→IRS1 while stating their data do not establish that edge uniquely.	D
Mathematical modeling of dietary timing- and protein quality-responsive liver circadian clock and its function on ribosome biogenesis LU2026 · DOI: 10.1152/physiolgenomics.00152.2026	Lu L; Androulakis IP et al. (2026)	Treats mTORC1 as a rhythm set by the timing and quality of amino acid intake rather than a fixed level, and asks what the shape of that rhythm does to ribosome biogenesis. A prediction, not a measurement — the model is in silico.	D

Upcoming events — where mTOR research is presented

The field has no meeting of its own. mTOR work is dispersed across autophagy, metabolism, cancer, geroscience and disease-foundation venues — basic science and human evidence in separate rooms. This calendar tracks both, from 2025 forward.

Each entry carries a tier:

Tier 1 mTOR is a named subject of the programme, or the meeting’s disease is mTOR.
Tier 2 a major recurring theme alongside adjacent biology.
Tier 3 relevance inferred from who attends, not what the programme says. Recorded, not prioritised.

Where programmes are published, speakers who are also Atlas authors are linked — click a name to open them in the Authors tab.

Click a conference to expand its details.

Upcoming & confirmed

▸6–11 Sep 2026EMBO Workshop: Autophagy — Foundations, Functions and Physiology 2026 Grenå, Denmark
EMBOUpcoming
6–11 Sep 2026 Grenå, DenmarkKysthotellet, Grenå
EMBO Workshop focused on the latest advances in autophagy mechanism and selective autophagy, including roles in metabolism, immunity, and cell differentiation. Organizer: Fulvio Reggiori (Aarhus University).
Why it matters for mTOR
TIER 2 — mTOR is a primary regulator of autophagy induction; speakers including Roberto Zoncu (lysosome/mTOR) ensure direct Atlas relevance. Sessions cover autophagy–mTOR crosstalk in metabolism and disease.
Organizers
Organized by: Fulvio Reggiori (Aarhus University), Lisa Frankel, Ian Ganley, Alexandra Stolz. (Updated 2026-07-26: full organizer team now published; previously only Reggiori was listed.)
Speakers
Ian Ganley, Sharon Tooze, Roberto Zoncu, Katja Simon, Louis Lapierre, Carine Joffre
Speakers in the Atlas (authors)
Ganley IGZoncu R
Conference site →
▸22–26 Sep 2026CSHL: Mechanisms of Aging 2026 Cold Spring Harbor, NY, USA
CSHLUpcoming
22–26 Sep 2026 Cold Spring Harbor, NY, USACold Spring Harbor Laboratory
CSHL meeting on the regulation and function of genes and processes known or suspected to control cellular and organismal aging.
Why it matters for mTOR
TIER 2 — Nutrient-sensing longevity pathways (TOR/AMPK/insulin-IGF) are central; organizer William Mair studies TOR/AMPK control of aging in C. elegans - directly adjacent to the Atlas.
Organizers
Organizers: Rozalyn Anderson (Univ. Wisconsin–Madison); William Mair (Harvard T.H. Chan); Ashley Webb (Buck Institute).
Speakers
Keynote: Rafael de Cabo (NIA). Confirmed invited speakers: Joseph Baur, Andreas Beyer, Jens Brüning, Weiwei Dang, Jennifer Elisseeff, Judith Frydman, Vadim Gladyshev, Margaret Goodell, Catherine Kaczorowski, Caroline Kumsta, Dudley Lamming, Jodi Nunnari, Courtney Marie Peterson, Marissa Schafer, Ming Xu. Organizers: Rozalyn Anderson, William Mair, Ashley Webb.
Speakers in the Atlas (authors)
Lamming DW
Conference site →
▸27–29 Sep 20267th European Meeting on AMPK & Nutrient-Sensing Pathways 2026 Lunteren, Netherlands
OtherUpcoming
27–29 Sep 2026 Lunteren, Netherlands
Triennial European meeting on AMPK and nutrient-sensing signalling. Published program includes dedicated sessions 'Beyond AMPK: nutrient-sensing pathways in health and diseases', 'AMPK family in cancer, aging and longevity', and 'AMPK and nutrient sensors in organelle biology'.
Why it matters for mTOR
TIER 2 — AMPK is the principal upstream antagonist of mTORC1: it inhibits mTORC1 both directly (Raptor Ser792) and via TSC2, the exact wiring already in the Atlas corpus (Shaw / Inoki / Gwinn). The program's explicit 'Beyond AMPK: nutrient-sensing pathways' and 'AMPK family in cancer, aging and longevity' sessions cover mTOR as the reciprocal arm of energy sensing. UPDATE (2026-07-22): official speaker list is now published and does NOT include Hardie or Shaw as previously speculated; confirmed speakers instead include Atlas authors Hongbo Chi (immunometabolism/AMPK-mTOR crosstalk in T cells) and Thomas Weichhart (mTOR/immunometabolism), both re-linked below in place of Shaw RJ.
Organizers
European AMPK community (organised via atoutcom.com/ampk); linked to EU-METAHEART COST Action CA22169
Speakers
Official speaker list published (atoutcom.com/ampk/speakers, as of 2026-07-20). Keynote speakers: Hongbo Chi (St. Jude Children's Research Hospital, USA), Kei Sakamoto (Novo Nordisk Foundation Center for Basic Metabolic Research, Copenhagen, Denmark). Invited speakers: Elena Baena-Gonzalez (Oxford), Olga Barca-Mayo (Santiago de Compostela), Julien Courchet (Univ. Claude Bernard Lyon 1), Bart Everts (Leiden UMC), Madelon Maurice (UMC Utrecht), Lykke Sylow (Univ. of Copenhagen), Thomas Weichhart (Medical Univ. of Vienna). Other confirmed speakers: Luc Bertrand (UC Louvain), Morgan Fullerton (Univ. of Ottawa), Remi Mounier (Univ. Claude Bernard Lyon 1), Ganna Panasyuk (Institut Necker Enfants Malades).
Speakers in the Atlas (authors)
Chi HWeichhart T
Conference site →
▸1–2 Oct 2026Animal Longevity Summit (ALOS) 2026 — Inaugural Toronto, Canada
OtherUpcoming
1–2 Oct 2026 Toronto, Canada
First dedicated international scientific conference on aging and healthspan in animals (canine-focused, animal-wide scope). Eight tracks: canine longevity, comparative biology of aging, model/non-model organisms, biomarkers/aging clocks, longevity interventions, veterinary geroscience, cross-species translation, early-career research.
Why it matters for mTOR
TIER 2 — Cross-species geroscience forum featuring leading mTOR/aging researchers (e.g. Matt Kaeberlein of the Dog Aging Project); companion-animal aging interventions are directly relevant to mTOR/rapamycin translational research (rapamycin dog aging trials). Not the sole subject of the meeting, but a named, substantive intervention class under discussion, not just inferred mechanistic adjacency.
Organizers
Vyom Goel (Founder, Animal Longevity Summit)
Speakers
Matt Kaeberlein (Dog Aging Project); Vera Gorbunova (University of Rochester); Aubrey de Grey (LEV Foundation); Varun Dwaraka (TruDiagnostic); Liz Parrish (BioViva); Raghav Sehgal (Yale) — additional speakers to be announced
Speakers in the Atlas (authors)
Kaeberlein M
Conference site →
▸1–3 Oct 2026ARDD 2026 — Aging Research and Drug Discovery (13th) Boston/Cambridge, MA, USA
ARDDUpcoming
1–3 Oct 2026 Boston/Cambridge, MA, USADavid Rubenstein Treehouse, Harvard University
The 13th Aging Research & Drug Discovery (ARDD) meeting -- flagship translational geroscience conference now organized by Insilico Medicine, relocated for 2026 to Harvard University. Tracks: Clinical Development/Longevity Medicine (Oct 1), AI in Drug Discovery (Oct 2), Future Technology (Oct 3).
Why it matters for mTOR
TIER 2 — As with prior editions, rapamycin/mTOR-based interventions are a core geroscience topic; a key future venue to track for mTOR translational work.
Organizers
Organized by Insilico Medicine. Chairs: Vadim Gladyshev (Executive Chair, Harvard Medical School); Jesse Poganik (Co-Chair, Harvard Medical School); Alex Zhavoronkov (Co-Chair, Insilico Medicine); Morten Scheibye-Knudsen (Co-Chair, Univ. of Copenhagen); Daniela Bakula (Co-Chair, Univ. of Copenhagen); Evelyne Bischof (Longevity Medicine Co-Chair, Sheba Longevity Center); Maximilian Unfried (AI in Drug Discovery Track Co-Chair, National Univ. of Singapore). Tier 1 sponsors include Eli Lilly.
Speakers
More speakers to be announced as of July 2026 (per official site).
Conference site →
▸4–6 Oct 2026Cell Symposia: Hallmarks of Aging 2026 Seville, Spain
Cell SymposiaUpcoming
4–6 Oct 2026 Seville, SpainMelia Sevilla Hotel
Cell Press Symposium exploring the cellular and molecular hallmarks of aging — from metabolism and disease to gerotechnology and gerotherapeutics.
Why it matters for mTOR
TIER 2 — Deregulated nutrient sensing (mTOR, AMPK, IIS) is a canonical hallmark of aging; organizers include caloric-restriction (de Cabo) and autophagy (Cuervo) leaders whose work overlaps mTOR biology.
Organizers
Organizers: Rafael de Cabo (NIA); Ana Maria Cuervo (Albert Einstein); Cell Press editors Mari-Carmen Fernandez-Aguera (Cell Metabolism), Novella Guidi (Cell Reports), Amber Mueller (Cell). Keynote: Luigi Ferrucci (NIA). (Updated 2026-07-26: named Cell Press editors now published, previously generic.)
Speakers
Keynote Luigi Ferrucci; confirmed speakers include Berenice Benayoun, Haim Cohen, Dolores Corella, Clara Correia-Melo, Vishwa Deep Dixit, David Glass, Mari-Carmen Gomez-Cabrera, among others.
Conference site →
▸5–6 Oct 20262026 Biomarkers of Aging Conference Boston, MA, USA
OtherUpcoming
5–6 Oct 2026 Boston, MA, USAJoseph B. Martin Conference Center, Harvard Medical School
Annual conference from the Biomarkers of Aging Consortium convening geroscience researchers to advance standardized, clinically validated biomarkers of aging and assess longevity intervention outcomes.
Why it matters for mTOR
TIER 3 — Broad geroscience/biomarkers meeting; several speakers (Gladyshev, Verdin, Rando, Gorbunova, Horvath) work on nutrient-sensing and metabolic longevity pathways adjacent to the Atlas's mTOR-aging axis, though the program itself is not mTOR-specific. Downgraded to Tier 3: relevance rests on speaker affiliation rather than program content — no mTOR session, no mTOR-titled talk. Retained for completeness, not prioritised.
Organizers
Conference Chairs: Vadim Gladyshev, Mahdi Moqri, Chiara Herzog, Andrea Cipriano, Jesse Poganik.
Speakers
Omar Abudayyeh, Maxim Artyomov, Dan Belsky, Heike Bischoff-Ferrari, Martin Borch Jensen, Ed Boyden, Peter Fedichev, Jennifer Garrison, Vadim Gladyshev, Vera Gorbunova, Clare Gustafson, Steve Horvath, Michael Levin, João Pedro de Magalhães, Samantha Morris, Thomas Rando, Birgit Schilling, Vittorio Sebastiano, Mike Snyder, Eric Verdin.
Conference site →
▸12–14 Oct 202613th CFATG Scientific Days on Autophagy (Paris) 2026 Paris, France
OtherUpcoming
12–14 Oct 2026 Paris, FranceFIAP Jean Monnet, 14th arrondissement
Annual meeting of the French Association for Autophagy Research (CFATG), featuring invited international keynote speakers and abstract-selected talks and posters. Abstract and early-bird registration deadline: July 31, 2026.
Why it matters for mTOR
TIER 2 — Features keynote Roberto Zoncu (UC Berkeley — leading mTOR/lysosome researcher and mTOR-autophagy axis expert), Sharon Tooze (Crick Institute, autophagy initiation upstream of mTOR), and Ian Ganley (mitophagy). Direct mechanistic overlap with Atlas autophagy-mTOR studies.
Organizers
CFATG Organizing Committee: Guillaume Beauclair, Aurore Claude-Taupin, Audrey Esclatine, Pierre-Emmanuel Joubert, Delphine Judith, Mojgan Djavaheri-Mergny, Etienne Morel. (Updated from official site; corrects earlier abbreviated organizer list.)
Speakers
Ian Ganley, Carine Joffre, Louis Lapierre, Katja Simon, Sharon Tooze, Roberto Zoncu
Speakers in the Atlas (authors)
Ganley IGZoncu R
Conference site →
▸14–16 Oct 20261st EFAR Conference on the Biology of Aging 2026 Cologne, Germany
OtherUpcoming
14–16 Oct 2026 Cologne, GermanyMPI for Biology of Ageing & CECAD Research Center
Inaugural conference of the newly founded European Federation for Aging Research (EFAR), which unites the German (DGfA), Dutch (DUSRA), Nordic, and British (BSRA) national aging-research societies to foster cross-European collaboration, funding coordination, and knowledge exchange in aging biology.
Why it matters for mTOR
TIER 3 — General aging-biology conference (cellular senescence, DNA repair, healthspan, geroscience) featuring Linda Partridge, a leading dietary-restriction/longevity signaling researcher already represented in the Atlas corpus, plus other senior aging-mechanism researchers. mTOR is not a named subject of the programme; relevance is inferred from who attends.
Organizers
Björn Schumacher (chair, Cologne); David Vilchez (Cologne); Anne Schaefer (Cologne); Morten Scheibye-Knudsen (Denmark); Lene Rasmussen (Denmark); Folkert Kuipers (Netherlands); Joris Deelen (Netherlands); Riekelt Houtkooper (Netherlands); David Weinkove (UK); Hartmut Geiger (Germany); Helen Morrison (Germany); Ira Milosevic (Portugal/UK)
Speakers
George Garinis; Laura Niederhofer; Linda Partridge; Luca Scorrano; Uri Alon; Sara Hägg; Lumír Krejčí; Nathan LeBrasseur; Elsa Longarinho; Matthias Mann; Eija Pirinen; Eline Slagboom; Guido Kroemer; Wojciech Pokrzywa; Emma Teeling
Speakers in the Atlas (authors)
Partridge L
Conference site →
▸2–3 Dec 2026Fifth Geroscience Summit: Revisiting the Geroscience Hypothesis - Focus on Health Bethesda, MD, USA
OtherUpcoming
2–3 Dec 2026 Bethesda, MD, USANIH Main Campus, Building 35
NIA-hosted summit (with the NIH Geroscience Interest Group) bringing together academic and industry researchers, clinicians, and other stakeholders in geroscience across 8 sessions to assess the state of the science, identify gaps, and build a 3-5 year research roadmap focused on healthspan.
Why it matters for mTOR
TIER 2 — NIH/NIA's flagship cross-institute geroscience summit. Gerotherapeutic development, hallmarks-of-aging biology, and healthspan biomarker sessions directly track the Atlas's nutrient-sensing/mTOR-aging axis; Session V (Gerotherapeutics for Health, Clinical Trials) and Session VII (New Initiatives in Geroscience) are the most mTOR/rapamycin-adjacent.
Organizers
NIH/NIA Geroscience Interest Group (GSIG). Welcome: Jay Bhattacharya (NIH Director), Richard Hodes (NIA Director). Session chairs: Juan Carlos Izpisua Belmonte, Jesse Poganik, Eileen Crimmins, John Beard, John Newman, Siobhan Malany, Jodi Nunnari, Elizabeth Necka. Overall moderators: Felipe Sierra, Vadim Gladyshev, Tony Wyss-Coray.
Speakers
Keynote: Luigi Ferrucci. Session I: Juan Carlos Izpisua Belmonte, Thomas Rando, George Kuchel, Guanghui Liu. Session II: Jesse Poganik, Yousin Suh, Paola Sebastiani. Session III: Eileen Crimmins, Cathal McCrory, Jessica Faul, Dana Goldman, Andrew Scott. Session IV: Daniel Belsky, Jennifer Brach, Su-In Lee, Michael Snyder. Session V: John Newman, Heinrich Jasper, James Peyer, Brianna Stubbs. Session VI: Warren Casey, Kristen Brennand, Joseph Wu, Luiz Eduardo Bertassoni, Francesca Duncan. Session VII: Jamie Justice, Joan Mannick, Andrew Brack. Session VIII: TBD. Roundtable participant: Steven Austad.
Speakers in the Atlas (authors)
Mannick JB
Conference site →
▸3–5 Feb 2027SEFAGIA Meeting 2027 Alfara del Patriarca (Valencia), Spain
OtherUpcoming
3–5 Feb 2027 Alfara del Patriarca (Valencia), Spain
Biennial-ish meeting of the Sociedad Española de Autofagia (SEFAGIA, Spanish Society of Autophagy), gathering autophagy and related-field researchers for several days of cutting-edge science, collaboration, and networking. Prior editions (SEFAGIA 2024, 2025) featured keynotes such as Robbie Loewith, Marja Jäättelä, and Terje Johansen.
Why it matters for mTOR
TIER 2 — Confirmed keynotes Ana Maria Cuervo (Albert Einstein College of Medicine — chaperone-mediated autophagy and lysosomal-mTORC1 crosstalk pioneer), Ivan Đikić (Goethe University Frankfurt — ubiquitin-autophagy signaling), and Nektarios Tavernarakis (University of Crete — autophagy and aging, C. elegans). Direct mechanistic overlap with the Atlas's mTORC1-lysosome-autophagy axis.
Organizers
Sociedad Española de Autofagia (SEFAGIA); named organizing/scientific committee for the 2027 edition not yet publicly posted.
Speakers
Ana Maria Cuervo, Ivan Đikić, Nektarios Tavernarakis (confirmed international keynotes; full speaker roster not yet public)
Conference site →
▸8–11 Feb 2027Keystone Symposia: Autophagy in Health and Disease — From Mechanisms to Therapeutics 2027 Banff, AB, Canada
Keystone SymposiaUpcoming
8–11 Feb 2027 Banff, AB, CanadaFairmont Banff Springs
Keystone Symposium (joint with 'Induced Proximity and Targeted Protein Degradation') covering core autophagy machinery, selective autophagy, non-canonical autophagy pathways, and therapeutic exploitation of autophagy including AUTACs.
Why it matters for mTOR
TIER 2 — mTORC1 is the principal negative regulator of autophagy initiation; sessions on lysosomal integration of biosynthetic/catabolic signaling (Zoncu) and autophagy in aging (Boya, Simon) are directly relevant to the Atlas's mTOR-autophagy-aging axis.
Organizers
Scientific Organizers: Hong Zhang, Susan Ferro-Novick, Hitoshi Nakatogawa.
Speakers
Keynote: Noboru Mizushima. Invited: Hitoshi Nakatogawa, Sascha Martens, Nobuo N. Noda, Susan Ferro-Novick, Florian Wilfling, Eric H. Baehrecke, Ana Maria Cuervo, Hong Zhang, Xiaochen Wang, Roberto Zoncu, Vojo Deretic, Yan Zhao, Mondira Kundu, Dimitri Krainc, Patricia Boya, Ai Yamamoto, Anna Katharina Simon, Boxun Lu, Vassiliki Nikoletopoulou.
Speakers in the Atlas (authors)
Zoncu RMizushima NKundu M
Conference site →
▸7–10 Mar 2027Keystone Symposia: Tumor and Host Metabolism — Integrating Molecular, Cellular, and Systemic Interactions 2027 Princeton, NJ, USA
Keystone SymposiaUpcoming
7–10 Mar 2027 Princeton, NJ, USALudwig Institute Princeton University
Keystone Symposium, presented in partnership with the Ludwig Institute for Cancer Research (Princeton Branch), on interactions between tumor and host metabolism: how environmental and whole-body changes, diet, and aging affect tumor growth and progression.
Why it matters for mTOR
TIER 2 — Successor to the Atlas's existing 'Tumor Metabolism' Keystone entry (2026). Direct mTORC1 relevance via Andrea Ballabio's confirmed talk 'Paracrine Activation of mTORC1 in the Tumor Microenvironment'; a dedicated Day-3 session ('Frontiers in Stress Responses and Aging in Cancer') covers aging-cancer metabolic crosstalk. Co-organized by Marcia Haigis (Co-Director, Paul F. Glenn Center for the Biology of Aging at Harvard) and Lydia Lynch (Princeton/Ludwig).
Organizers
Scientific Organizers: Marcia C. Haigis (Harvard Medical School); Lydia Lynch (Princeton University).
Speakers
Keynote: Karen H. Vousden (Francis Crick Institute). Confirmed speakers: Semir Beyaz (CSHL), Ruaidhri P. Jackson (Harvard Medical School), Michael Skinnider (Princeton), Garry P. Nolan (Stanford), Joshua D. Rabinowitz (Princeton), Stacey D. Finley (USC), Hongbo Chi (St. Jude), Leeat Keren (Weizmann Institute), Andrea Ballabio (Telethon Institute of Genetics and Medicine), Luke A. J. O'Neill (Trinity Biomedical Sciences Institute), Lydia Lynch (Princeton), Alison Ringel (MIT), Marcia C. Haigis (Harvard), Ashani T. Weeraratna (Johns Hopkins), Sarah-Maria Fendt (VIB-KU Leuven), Noga Ron-Harel (Technion), Jonathan D. Powell (Calico Life Sciences), Ping-Chih Ho (Ludwig Institute), Carl H. June (UPenn).
Speakers in the Atlas (authors)
Chi HBallabio APowell JD
Conference site →
▸21–24 Mar 2027Keystone Symposia: Integrative Mitochondrial Medicine 2027 Banff, Canada
Keystone SymposiaUpcoming
21–24 Mar 2027 Banff, CanadaFairmont Banff Springs
Keystone Symposia conference on integrative mitochondrial medicine, spanning mitochondrial genome editing, synthetic biology, imaging, precision medicine for mitochondrial disease, and mitochondrial transplantation.
Why it matters for mTOR
TIER 3 — Mitochondrial quality control, biogenesis and dynamics are tightly coupled to mTOR/AMPK nutrient-sensing signaling (mitophagy, PGC-1alpha-driven biogenesis); direct companion event to the Atlas's existing 'Mitochondria Signaling in Physiology and Disease' Keystone meeting. Same basis as that entry: mTOR is not a named program topic, the connection is inferred mechanistic adjacency. Retained for completeness, not prioritised.
Organizers
Nils-Goran Larsson (Karolinska Institutet); Aleksandra Filipovska (University of Western Australia)
Speakers
Vamsi K. Mootha; Wendy Shoop; Min Jiang; Carlos T Moraes; Oliver Rackham; Martin Fussenegger; Aleksandra Filipovska; Danielle Grotjahn; Antentor O Hinton Jr.; Gulcin Pekkurnaz; Elisa Motori; Claes Gustafsson; Thomas Keating; Michio Hirano; Christian Frezza; Nils-Goran Larsson; Natalie Niemi; Jared Rutter; Robert McFarland; Janine Santos; Heidi M. McBride
Conference site →
▸2–7 Apr 2027AACR Annual Meeting 2027 Orlando, FL, USA
OtherUpcoming
2–7 Apr 2027 Orlando, FL, USAOrange County Convention Center
The largest cancer research meeting in the world, spanning basic, translational and clinical oncology.
Why it matters for mTOR
TIER 2 — The principal venue where human data on mTOR-pathway inhibitors surface first. Rapalog resistance mechanisms, PI3K-AKT-mTOR biomarker work, and the clinical development of third-generation mTOR inhibitors are all reported here. Added to correct a structural bias in this table: the mTOR evidence base is heavily basic-science and geroscience, while the human evidence that the Atlas's translation-gap thesis depends on is adjudicated in oncology.
Organizers
American Association for Cancer Research (AACR)
Speakers
Program not yet published; Linked_Authors left blank until speakers are confirmed.
Conference site →
▸12–15 Apr 2027Keystone Symposia: Healthy Aging & Therapeutic Opportunities 2027 Taipei, Taiwan
Keystone SymposiaUpcoming
12–15 Apr 2027 Taipei, TaiwanNTUH International Convention Center
Keystone Symposia conference examining emerging strategies for promoting healthy aging, with a focus on biomarkers of aging, therapeutic development, and interventions to improve quality of life. Sessions cover geromedicine, biomarkers of aging, non-pharmacologic approaches, combination therapies, drug target identification, and translational/regulatory challenges.
Why it matters for mTOR
TIER 2 — Co-organized by Brian K. Kennedy, a leading rapamycin/mTOR and NAD+ longevity researcher; geromedicine and combination-therapy sessions are directly adjacent to the Atlas's mTOR-intervention focus.
Organizers
Scientific Organizers: Derek Huffman (Albert Einstein College of Medicine); Kristen Fortney (BioAge Labs); Brian K. Kennedy (National University of Singapore); Shu-Chun Teng (National Taiwan University).
Speakers
Confirmed speaker roster not yet published as of July 2026; organizers listed above.
Speakers in the Atlas (authors)
Kennedy BK
Conference site →
▸16–21 May 2027Gordon Research Conference: Lysosomal Diseases 2027 Les Diablerets, Switzerland
Gordon Research ConferenceUpcoming
16–21 May 2027 Les Diablerets, SwitzerlandLes Diablerets Conference Center / Eurotel Victoria
GRC on Lysosomal Diseases, themed "Understanding Lysosomes to Enable Innovative Therapies". Five-day closed meeting on unpublished work spanning fundamental lysosomal biology and therapy development for lysosomal storage disorders. Preceded by the associated Gordon Research Seminar (15-16 May 2027). Application deadline 18 April 2027.
Why it matters for mTOR
TIER 3 — Indirect but real: the lysosomal surface is the platform on which mTORC1 is activated (Rag GTPases, Ragulator/LAMTOR, v-ATPase), and mTORC1 in turn controls the TFEB/TFE3 lysosomal-biogenesis program. Lysosomal-storage-disease biology and mTORC1-TFEB signalling are studied by overlapping groups (e.g. Ballabio, Zoncu, Ferguson, Settembre). Scope note: this is a lysosome-biology meeting, not an mTOR-centred one — mTOR content will be a subset of the program. Tier is provisional: the programme is unpublished as of 2026-08-15 (due 19 August 2026), so relevance is currently inferred from the community rather than from stated sessions; revisit for a possible TIER 2 once sessions are announced.
Organizers
Chairs and vice-chairs not yet published by GRC as of 2026-08-15; preliminary program with invited speakers due 19 August 2026.
Speakers
Not yet announced — GRC publishes the speaker list with the preliminary program (expected 19 August 2026).
Conference site →
▸16–19 May 20276th Interventions in Aging Conference 2027 Durrës, Albania
OtherUpcoming
16–19 May 2027 Durrës, AlbaniaMeliá Durrës
Long-running (6th edition, since 2015) small-format geroscience conference on molecular/cellular mechanisms of aging and translation into human interventions — exercise, chronobiology, tissue-specific aging biomarkers, genetic variation, and systems biology approaches to healthy aging.
Why it matters for mTOR
TIER 2 — Core geroscience meeting chaired by leading nutrient-sensing/aging researchers (Linda Partridge, Heinrich Jasper, William Mair — all with major contributions to TOR/insulin-IGF1 longevity pathway work); sessions on pharmacological and lifestyle interventions targeting core aging mechanisms directly overlap the Atlas's mTOR/geroscience scope. Rapamycin/mTOR inhibition is a recurring theme in aging-intervention pharmacology alongside adjacent biology, as at ARDD.
Organizers
Linda Partridge (UCL); Heinrich Jasper (Genentech); William Mair (Harvard)
Speakers
Rafael de Cabo; Leanne Jones; Andrea Maier; Tony Wyss-Coray; Salvador Aznar-Benitah; Heike Bischoff-Ferrari; Ed Chouchani; Luigi Ferrucci; Chiara Herzog; Mika Kivimaki; Nathan LaBrasseur; Courtney Peterson; Daniel Promislow; Nicholas Stroustrup; Dario Valenzano
Speakers in the Atlas (authors)
Partridge L
Conference site →
▸17–21 May 2027CSHL: Mechanisms of Metabolic Signaling 2027 (8th) Cold Spring Harbor, USA
CSHLUpcoming
17–21 May 2027 Cold Spring Harbor, USACold Spring Harbor Laboratory
The eighth Cold Spring Harbor Laboratory meeting on Mechanisms of Metabolic Signaling & Disease, bringing together researchers spanning biochemistry, molecular biology, physiology, and pathophysiology to define the role and regulation of metabolic signals across pathways, cell types, and disease states.
Why it matters for mTOR
TIER 2 — Core CSHL metabolic-signaling meeting with dedicated sessions on 'Metabolic Signaling' and 'Metabolism, Growth, and Proliferation' — directly overlapping mTOR/nutrient-sensing biology; comparable in scope to the already-curated CSHL: Mechanisms of Aging meeting. mTOR is a major recurring theme alongside adjacent metabolic signalling, rather than a named headline subject.
Organizers
Bart Deplancke (EPFL, Switzerland); Sarah-Maria Fendt (VIB Leuven, Belgium); Deborah Muoio (Duke University School of Medicine)
Speakers
Conference site →
▸4–8 Jun 2027ASCO Annual Meeting 2027 Chicago, IL, USA
OtherUpcoming
4–8 Jun 2027 Chicago, IL, USAMcCormick Place Convention Center
The largest clinical oncology meeting worldwide; where practice-changing trial results are first presented.
Why it matters for mTOR
TIER 2 — Where mTOR inhibition meets clinical endpoints in humans. The everolimus registration trials (RECORD-1 in renal cell carcinoma, BOLERO-2 in breast cancer, RADIANT-3 in neuroendocrine tumours - Motzer RJ, Baselga J, Yao JC, all Atlas authors) were reported at ASCO, as were the RMC-5552 combination findings. The purest expression of the Atlas's translation-gap axis: mTOR inhibitors that work in mice tested against hard human endpoints.
Organizers
American Society of Clinical Oncology (ASCO)
Speakers
Program not yet published; Linked_Authors left blank until speakers are confirmed.
Conference site →
▸5–9 Jun 2027American Transplant Congress (ATC) 2027 Seattle, WA, USA
OtherUpcoming
5–9 Jun 2027 Seattle, WA, USAWashington State Convention Center
Joint annual meeting of the American Society of Transplantation (AST) and the American Society of Transplant Surgeons (ASTS); >4,000 attendees. (ATC 2026, Boston, 20-24 June 2026, has already passed.)
Why it matters for mTOR
TIER 2 — Transplantation is the largest human exposure dataset in existence for sirolimus and everolimus (approved for rejection prophylaxis long before any geroscience trial) and the origin of the canonical adverse-effect profile the Atlas records: hyperlipidaemia, insulin resistance and new-onset diabetes, impaired wound healing, mucositis, infection. Supplies the human safety denominator that geroscience trials cite second-hand. Atlas authors in this space: Budde K, Saemann MD, Singer LG.
Organizers
American Society of Transplantation (AST) and American Society of Transplant Surgeons (ASTS)
Speakers
Program not yet published; Linked_Authors left blank until speakers are confirmed.
Conference site →
▸25–30 Jul 2027Gordon Research Conference: Biology of Aging 2027 Lucca (Barga), Italy
Gordon Research ConferenceUpcoming
25–30 Jul 2027 Lucca (Barga), ItalyRenaissance Tuscany Il Ciocco
Long-running (since 1962) flagship Gordon Research Conference on the biology of aging, held biennially, alternating US/Europe venues. Brings together the core international aging-biology research community across molecular, cellular, and organismal scales.
Why it matters for mTOR
TIER 2 — mTOR/nutrient-sensing signaling (rapamycin, TOR pathway, autophagy) has been a recurring major session theme at prior editions of this conference given its central role in aging biology; a flagship venue for mTOR-and-aging primary research even when not named in the title.
Organizers
Speakers
Conference site →
▸26–30 Oct 2027AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics 2027 Chicago, IL, USA
OtherUpcoming
26–30 Oct 2027 Chicago, IL, USASheraton Grand Chicago Riverwalk
Small, drug-development-focused conference jointly organised by AACR, the NCI and the EORTC; the main venue where first-in-human data on novel targeted agents are reported before journal publication.
Why it matters for mTOR
TIER 2 — Direct provenance for the Atlas's own Schram 2025 entry: the first-in-human phase 1/1b data for RMC-5552, the first bi-steric mTORC1-selective inhibitor in the clinic, were presented here (Abstract C020, 2023) before the Clinical Cancer Research paper. This is where Open Question 2 (inhibit mTORC1 without affecting mTORC2) is being answered in humans rather than in mice: bi-steric selectivity relieves the mTORC2-mediated hyperglycaemia that limited earlier pan-mTOR inhibitors. Also the venue for 4E-BP1 pharmacodynamics and mucositis management.
Organizers
AACR, NCI, EORTC
Speakers
2027 program not yet published; Linked_Authors left blank until speakers are confirmed.
Conference site →

Past

▸30 Jul – 1 Aug 20262026 TSC World Conference Aurora, CO, USA
OtherPast
30 Jul – 1 Aug 2026 Aurora, CO, USAGaylord Rockies Resort & Convention Center
Held every four years by the TSC Alliance, co-hosted with Tuberous Sclerosis Complex International (TSCi). ~1,000 participants and ~45 sessions spanning research, clinical care, and family programming.
Why it matters for mTOR
TIER 1 — TSC is the genetic disease that established the TSC1/TSC2 -> Rheb -> mTORC1 axis, and the only indication where an mTOR inhibitor (everolimus) is approved on a directly genetic mTOR rationale (EXIST-1/-2/-3). Anchors the human side of the Atlas's Clinic branch. Atlas authors carrying this evidence: Franz DN, Krueger DA, Bissler JJ, Jozwiak S, Kingswood JC, Bebin EM, Sparagana S, Zonnenberg BA, Belousova E. CAVEAT: mixed research/family conference, not a pure scientific meeting; the TSC Alliance also runs a research-only International TSC Research Conference in off-years, worth tracking separately.
Organizers
TSC Alliance, co-hosted with Tuberous Sclerosis Complex International (TSCi)
Speakers
Speaker list not yet resolved against the Atlas Authors table; Linked_Authors deliberately left blank until the program publishes.
Conference site →
▸24–27 Jun 2026Prague Metabolism and Signaling Symposium 2026 Prague, Czech Republic
Prague Metabolism SymposiumPast
24–27 Jun 2026 Prague, Czech RepublicNational Library of Technology (NTK), Campus Dejvice
Meeting bringing together experts at the intersection of metabolism and signal transduction. ~30 invited speakers plus two keynotes, with short talks and poster sessions. Chaired by David Sabatini (IOCB Prague/Boston) and Katerina Rohlenova. A dedicated closing 'mTOR Biology' session features Brendan Manning, Kuang Shen, Mario Pende and David Sabatini, with Michael N. Hall (the discoverer of TOR) giving the second keynote.
Why it matters for mTOR
TIER 1 — Highest relevance in the calendar. Co-chaired by David Sabatini, keynote by Michael N. Hall (discovered TOR), and an explicit 'mTOR Biology' session. Many speakers are core mTOR/metabolism labs, several of whom are authors in the Atlas corpus.
Organizers
Chairs: Katerina Rohlenova (Institute of Biotechnology, Czech Academy of Sciences); David Sabatini (IOCB Prague & IOCB Boston). Keynotes: Karen Vousden (Francis Crick Institute); Michael N. Hall (Biozentrum, University of Basel).
Speakers
Keynotes: Karen Vousden, Michael N. Hall. Invited: Janelle Ayres, Liron Bar-Peled, Issam Ben Sahra, Kivanc Birsoy, Anne Brunet, Ralph DeBerardinis, Andrew Dillin, Alejo Efeyan, Mark Febbraio, Lydia Finley, Gerta Hoxhaj, Navdeep Chandel, Heather Christofk, Nada Kalaany, Naama Kanarek, Pekka Katajisto, Brendan Manning, Michael Pacold, Thales Papagiannakopoulos, Erika Pearce, Mario Pende, Richard Possemato, Jared Rutter, Luca Scorrano, Reuben Shaw, Kuang Shen, Celeste Simon, Jessica Spinelli, Eileen White, Omer Yilmaz.
Speakers in the Atlas (authors)
Sabatini DMHall MNBar-Peled LEfeyan AHoxhaj GKalaany NYManning BDShaw RJShen KBen-Sahra IBrunet A
Conference site →
▸14–19 Jun 2026Gordon Research Conference: Systems Aging 2026 Newry, Maine, USA
Gordon Research ConferencePast
14–19 Jun 2026 Newry, Maine, USAGrand Summit Hotel, Sunday River
Gordon Research Conference on Systems Aging — systems-level approaches to the biology of aging across species, evolution, reproduction, human longevity and frailty. A companion Gordon Research Seminar (GRS) ran June 13-14, 2026.
Why it matters for mTOR
TIER 2 — Nutrient-sensing and mTOR / insulin-IGF signaling are central pillars of systems-level aging biology featured at this meeting; directly relevant to the Atlas's mTOR-aging axis.
Organizers
Conference chair(s) not yet publicly listed as of July 2026; program under development per GRC site.
Speakers
Speaker list not yet published as of July 2026 — GRC states the detailed program (chair, speakers, discussion leaders) will be posted by Feb 14, 2026. Check https://www.grc.org/systems-aging-conference/2026/ for updates.
Conference site →
▸8–11 Jun 2026Keystone: Tumor Metabolism — New Frontiers in Diet, Microbiome and Beyond 2026 Killarney, Ireland
Keystone SymposiaPast
8–11 Jun 2026 Killarney, IrelandINEC Killarney Convention Centre
Keystone Symposium exploring the reciprocal relationship between cancer and whole-body metabolism, including diet, the microbiome, aging and metabolic disease.
Why it matters for mTOR
TIER 2 — The PI3K-AKT-mTOR axis is a central controller of tumor cell growth and metabolism; diet/nutrient inputs that shape tumor metabolism act largely through mTORC1.
Organizers
Scientific organizers: Karen H. Vousden; Cynthia L. Sears; Eileen White.
Speakers
Organizers: Karen H. Vousden, Cynthia L. Sears, Eileen White. Keynote: Heather Christofk. Invited/session speakers: Craig B. Thompson, Matthew G. Vander Heiden, Christopher Halbrook, Bertrand Routy, Saman Maleki, Navdeep S. Chandel, Ayelet Erez, Peter J. Mullen, Ralph J. DeBerardinis, Scott J. Dixon, Richard L. Possemato, Lydia Lynch, Marcus D. Goncalves, Thales Papagiannakopoulos, Mariia Yuneva, Oliver Maddocks, Yanxiang (Jessie) Guo.
Conference site →
▸5 Jun 2026mTOR Node Symposium 2026 (3rd Annual) London, UK
OtherPast
5 Jun 2026 London, UKKing's College London
Third annual research meeting of the UK mTOR Pathway Diseases node (NIHR/MRC-funded initiative), convening ~70 researchers, clinicians, industry representatives and patients around the 14 known rare diseases caused by mutations in mTOR-pathway genes (~10,000 people affected in the UK).
Why it matters for mTOR
TIER 1 — The only meeting in the calendar organized around mTOR-pathway diseases as its sole subject, not just an adjacent topic. Discovery-science session explicitly covered phosphoproteomics, EV biomarkers, patient-derived assembloids, cellular ageing models, and 'the broader relevance of mTOR signalling across rare and age-related diseases' — directly on-topic for the Atlas's clinic/translation branch. No named external invited-speaker roster was published in the public writeup (a PPIE patient/clinical meeting, not a standard academic program), so Linked_Authors is left empty; node leadership is captured in Organizers instead.
Organizers
Professor Joseph Bateman (lead investigator, Molecular Neuroscience, King's College London); Professor Deb Pal (Paediatric Epilepsy); Dr Laura Mantoan Ritter (Consultant Neurologist); Dr Frances Elmslie (Consultant Clinical Geneticist, St George's); Dr Charlotte Tye (Senior Lecturer in Psychology); Sylvine Lalnunhlimi Butvilauskiene (Research Project Manager).
Speakers
No public named external speaker roster; talks given by node investigators and NHS/registry partners. PPIE Advisory Panel patient representative: Melanie Levy.
Conference site →
▸2–5 Jun 2026AGE 54th Annual Meeting 2026 (American Aging Association) Provo, Utah, USA
OtherPast
2–5 Jun 2026 Provo, Utah, USAUtah Valley Convention Center
54th Annual Meeting of the American Aging Association (AGE). Theme: 'Geroscience: From Discovery to Application.'
Why it matters for mTOR
TIER 2 — Flagship US geroscience meeting; nutrient-sensing / mTOR biology and rapamycin-class interventions are recurring core topics.
Organizers
American Aging Association (AGE). Named lectures: Denham Harman Research Award (Steven Austad); AFAR/Cristofalo Award (Marianna Sadagurski); James Joseph/Mark Smith Award (Alberto Espay).
Speakers
Program speakers/chairs incl. Steven Austad (Denham Harman Award Lecture), Rafael de Cabo, Andrzej Bartke, Holly Brown-Borg, Alessandro Bitto (“mTOR inhibition bypasses loss of Complex I activity”), Vishwa Deep Dixit, Marianna Sadagurski (Cristofalo Award), Michael Olivier, Michal Masternak, Liou Sun, Nathan Basisty, Stacy Hussong, Kevin Koronowski, Sarah Ocanas, Cristal Hill. Full program (10 sessions): https://www.americanagingassociation.org/assets/images/2026Meeting/AGE%20Program%20060126.pdf
Speakers in the Atlas (authors)
Bartke ABrown-Borg HMBitto AHussong SA
Conference site →
▸25–27 May 2026International Autophagy Conference 2026 (Norwegian, German & UK Networks) Oslo, Norway
OtherPast
25–27 May 2026 Oslo, NorwayHolmen Fjordhotell
Joint international autophagy conference organized by three national autophagy research networks — ARCTiC (Norway), SFB1177 (Germany) and Autophagy UK — bringing together ~150 participants for a broad scientific program spanning autophagy molecular mechanisms, selectivity, organelle turnover, trafficking, protein homeostasis, autophagy in biology, human disease and therapeutic targeting.
Why it matters for mTOR
TIER 2 — core autophagy mechanism meeting; mTORC1 is the master negative regulator of autophagy and several sessions (organelle turnover, protein homeostasis, targeting autophagy) directly engage mTOR-autophagy crosstalk. Speaker roster overlaps heavily with the Atlas's existing autophagy/mTOR author base (Harper, Mizushima, Ganley).
Organizers
Anne Simonsen (Oslo), Ivan Dikic (Goethe/SFB1177), Sharon Tooze (Francis Crick), Harald Stenmark (Oslo), Tassula Proikas-Cezanne (Tubingen), Ian Ganley (Dundee).
Speakers
Sharon Tooze, Christian Behrends, Viola Nahse, Amos Liang, Helene Knaevelsrud, Brenda Schulman, Terje Johansen, Alexandra Stolz, Simon Wilkinson, Nikolai Engedal, Claudine Kraft, Rupert Beale, Wade Harper (keynote), Anne Simonsen, Ian Ganley, Gerhard Hummer, Anja Bremm, Harald Stenmark, Florian Wilfling, Sylvie Urbe, Christian Munch, Claudio Joazeiro, Alf Hakon Lystad, Dorothee Dormann, Jon Lane, Zvulun Elazar, Noor Gammoh, Tor Erik Rusten, Tassula Proikas-Cezanne, Li Yu, Noboru Mizushima (keynote), Katja Simon, Evandro Fei Fang, Vignir Helgason, Michael Potente, Bernadette Carroll, Jorrit Enserink, Paolo Grumati, Vojo Deretic (keynote)
Speakers in the Atlas (authors)
Harper JWMizushima NGanley IG
Conference site →
▸17–21 May 2026EMBO Workshop: Neuronal Autophagy — From Circuit Function to Therapy 2026 Sant Feliu de Guixols, Spain
EMBOPast
17–21 May 2026 Sant Feliu de Guixols, SpainHotel Eden Roc
EMBO Workshop on how autophagy integrates with neuronal signaling, metabolism, and disease mechanisms — proteostasis, mitochondrial quality control, synaptic remodeling, neurodegeneration. Follow-up to the 2022 EMBO Workshop 'Brain Autophagy in Health and Disease.'
Why it matters for mTOR
TIER 2 — Autophagy is a core mTORC1-regulated process; this workshop covers mTOR-linked neuronal proteostasis and autophagy dysfunction in neurodegeneration and aging-related decline, directly relevant to the Atlas's mTOR-autophagy axis.
Organizers
Speakers
Conference site →
▸21–25 Apr 2026CSHL: Protein Homeostasis in Health and Disease 2026 (17th) Cold Spring Harbor, NY, USA
CSHLPast
21–25 Apr 2026 Cold Spring Harbor, NY, USACold Spring Harbor Laboratory
17th edition of the CSHL meeting on proteostasis: chaperones, the unfolded protein response, co-translational folding and ribosome quality control, biomolecular condensates, and protein clearance via the autophagy-lysosomal pathway and the ubiquitin-proteasome system, with dedicated sessions on aging and neurodegeneration. Partly funded by the National Institute on Aging (grant 1R13AG099698-01).
Why it matters for mTOR
TIER 3 — mTOR is not a named session topic, but the meeting's "Degradation Mechanisms — Autophagy Lysosomal Pathway" and "Organellar Proteostasis and Spatial Quality Control in Aging" sessions sit directly downstream of mTORC1's control of autophagy and lysosomal biogenesis (TFEB). Aging-focused organizers (Malene Hansen, Buck Institute) and chairs (Ana Maria Cuervo, Anne Simonsen, Andrew Dillin) make it adjacent rather than central to the Atlas.
Organizers
Organizers: Judith Frydman (Stanford University); Malene Hansen (Buck Institute for Research on Aging); Ursula Jakob (University of Michigan).
Speakers
Session chairs / keynote speakers (CSHL does not publish a full talk roster in advance): F. Ulrich Hartl (MPI Biochemistry), Rick Morimoto (Northwestern), Veena Prahlad (Roswell Park), Ritwick Sawarkar (Cambridge), Rachel Klevit (Univ. Washington), Hideki Taguchi (Institute of Science Tokyo), Claudio Joazeiro (Heidelberg), Marina Rodnina (MPI Biochemistry), Christine Mayr (MSKCC), Florian Wilfling (MPI Biophysics), Ana Maria Cuervo (Albert Einstein), Anne Simonsen (Oslo), Andrew Dillin (UC Berkeley), Kazuhiro Nagata (Kyoto Sangyo), Marc Diamond (UT Southwestern), Aimee Kao (UCSF).
Conference site →
▸15–20 Mar 2026Gordon Research Conference: Autophagy in Stress, Development and Disease 2026 Ventura, CA, USA
Gordon Research ConferencePast
15–20 Mar 2026 Ventura, CA, USAVentura Beach Marriott
GRC on core autophagy machinery and its roles in cancer, aging, neurodegeneration, infectious disease and development.
Why it matters for mTOR
TIER 2 — mTORC1 is the master negative regulator of autophagy; this GRC directly covers the mechanistic and disease biology of the autophagy pathway central to the Atlas's autophagy/lysosome arm. Confirmed 2026 program includes a dedicated talk on "The TFEB-mTORC1 Axis in Tumorigenesis."
Organizers
Chairs and vice chairs confirmed on the GRC site as of the conference (Mar 15-20, 2026), but GRC renders names as images (anti-scraping), so they cannot be captured in text form. Conference has concluded; names remain unresolved from public text sources as of 2026-07-22.
Speakers
Conference site →
▸9–12 Feb 2026Keystone: Mitochondria Signaling in Physiology and Disease 2026 Keystone, Colorado, USA
Keystone SymposiaPast
9–12 Feb 2026 Keystone, Colorado, USAKeystone Resort
Keystone Symposium on mitochondria as signaling organelles that control cellular and organismal physiology, and how mitochondrial dysfunction drives disease.
Why it matters for mTOR
TIER 3 — Mitochondrial metabolism and nutrient status are tightly integrated with mTORC1 signaling; mitochondrial cues feed into growth control central to the Atlas. Downgraded to Tier 3: mTOR is not a named topic anywhere in the program — the connection is inferred adjacency (mitochondrial cues feeding nutrient sensing), not stated content. Retained for completeness, not prioritised.
Organizers
Scientific organizers: Navdeep S. Chandel; Aleksandra Trifunovic.
Speakers
Organizers: Navdeep S. Chandel, Aleksandra Trifunovic. Keynote: Anu Suomalainen Wartiovaara. Invited/session speakers: Elena Ziviani, Kivanc Birsoy, Dipayan Chaudhuri, Dustin Hancks, Xin Jie Chen, Phillip West, María Mittelbrunn, Lena Pernas, Michelle Clasquin, Andrew G. Dillin, Jose Antonio Enríquez, Peter M. Douglas, Dave Pagliarini, Prashant Mishra, Reuben J. Shaw, Jan Riemer, Marcia C. Haigis, Jay H. Chung, Janine Santos, Liron Bar-Peled, Mike P. Murphy.
Speakers in the Atlas (authors)
Bar-Peled LShaw RJ
Conference site →
▸2–5 Feb 2026Keystone: Autophagy — Mechanisms to Therapy 2026 Keystone, Colorado, USA
Keystone SymposiaPast
2–5 Feb 2026 Keystone, Colorado, USAKeystone Resort
Keystone Symposium covering the roles and mechanisms of autophagy across health and disease, spanning basic, translational and clinical research plus industry developments. Held jointly with the Keystone symposium 'Membrane Dynamics, Repair and Disease' to enable cross-talk.
Why it matters for mTOR
TIER 2 — mTORC1 is the master negative regulator of autophagy; sessions address mTOR inhibition and nutrient control of autophagic flux. Directly relevant to the autophagy/lysosome arm of the Atlas.
Organizers
Scientific organizers: Anne Simonsen; Sharon A. Tooze; Dan Baird.
Speakers
Organizers: Anne Simonsen, Sharon A. Tooze, Dan Baird. Keynotes: Erika L. Holzbaur, Harald Stenmark. Invited/session speakers: Felix Randow, Oliver Florey, Jayanta Debnath, Rupert Beale, Maho Hamasaki, Zvulun Elazar, J. Wade Harper, Phyllis Hanson, James H. Hurley, Claudio Bussi, Ivan Dikic, Ai Yamamoto, Joseph D. Mancias, Anastasia Henry, Chris Shoemaker, Simon Wilkinson, Michael Lazarou, Chantell S. Evans, Martin Graef.
Speakers in the Atlas (authors)
Hurley JHDebnath JHarper JW
Conference site →
▸26–28 Sep 2025International LAM Research Conference & LAMposium 2025 Kansas City, MO, USA
OtherPast
26–28 Sep 2025 Kansas City, MO, USAWestin Kansas City at Crown Center
The LAM Foundation's marquee event: a dual-track meeting combining a scientific research conference (>100 researchers and clinicians) with a patient and family conference; >300 attendees. Held every two to three years in rotating locations. NEXT EDITION NOT YET ANNOUNCED as of July 2026 - this record documents the 2025 edition; add the next edition when dated.
Why it matters for mTOR
TIER 1 — LAM is the second approved mTOR-inhibitor indication (sirolimus, via the MILES trial) and the only disease in the world whose standard of care IS mTOR inhibition. The single most concentrated venue for human sirolimus efficacy and long-term safety data. Atlas authors: McCormack FX, Moss J.
Organizers
The LAM Foundation
Speakers
Speaker list not resolved against the Atlas Authors table; Linked_Authors deliberately left blank.
Conference site →
▸25–29 Aug 2025ARDD 2025 — Aging Research and Drug Discovery (12th) Copenhagen, Denmark
ARDDPast
25–29 Aug 2025 Copenhagen, DenmarkCeremonial Hall, University of Copenhagen
The 12th Aging Research and Drug Discovery meeting — the largest translational geroscience conference — convening academics, biotech founders, pharma and clinicians over a five-day hybrid event on the biology of aging and drug development.
Why it matters for mTOR
TIER 2 — Rapamycin/mTOR inhibition is one of the central pillars of aging pharmacology; geroscience translation of mTOR is a recurring theme of ARDD and directly informs the Atlas gap/hypothesis layer.
Organizers
Organized by the University of Copenhagen (Scheibye-Knudsen group) and partners.
Speakers
Speakers/participants included David Sinclair (Harvard), Marco Demaria, Kristen Fortney (BioAge), Morten Meldal (Nobel laureate), Andrew Adams (Eli Lilly), among many others.
Conference site →
▸25–28 Jun 2025Keystone: Autophagosomes and Endolysosomes 2025 Whistler, BC, Canada
Keystone SymposiaPast
25–28 Jun 2025 Whistler, BC, CanadaFairmont Chateau Whistler
Keystone Symposium 'Autophagosomes and Endolysosomes: From Fundamental Mechanisms to Disease Implications', spanning the biogenesis and function of autophagosomes and the endolysosomal system through to disease.
Why it matters for mTOR
TIER 2 — The lysosomal surface is the physical platform for mTORC1 activation (Rag GTPases, Ragulator) and the TFEB axis; endolysosomal biology is core mechanistic ground for the Atlas.
Organizers
Scientific organizers: Christina Towers; Rupert Beale; Leon O. Murphy.
Speakers
Organizers/speakers: Christina Towers, Rupert Beale, Leon O. Murphy (full speaker list on the Keystone site).
Conference site →

Oliver's mTOR Atlas

Everything the landmark literature shows about mTOR — and everything it doesn’t

The evidence pyramid

Outside the evidence hierarchy

The mTOR pathway, mapped end to end.

Every study, sortable by tier and year.

All Studies

The people behind the papers.

All Authors

Where the evidence runs out.

What we don’t know — and why

InterpretationNutrient-sensor evidence desert

InterpretationHuman hard-endpoint desert

How mTOR biology actually grew

How we got here

The person and the project.

What this project is

What makes it different

How it's built and kept current

Editorial policy — how studies are chosen

Author

Oliver Barton

Related studies — Oliver's current focus

Upcoming events — where mTOR research is presented