Cognition
Learning, memory and related brain function. mTOR inhibition can enhance cognition in young mice and blunt age-related cognitive decline.
Learning, memory, and related brain function. Turning mTOR down can sharpen thinking in young mice and may soften age-related mental decline, though the same drugs also carry real risks for brain-cell signaling.
Learning, memory and related brain function. mTOR inhibition can enhance cognition in young mice and blunt age-related cognitive decline.
TL;DR. Cognition appears in 6 curated studies in Oliver's mTOR Atlas: 6 in animal models. No study in people is recorded for it in the Atlas yet.
Evidence at a glance
| Evidence | What it means | Studies |
|---|---|---|
| A | Animal model | 6 |
No direct human evidence in the Atlas for this entity yet — everything below rests on animal or molecular work.
Studies
| Year | Evidence | Study |
|---|---|---|
| 2026 | A | High-concentration hydrogen mitigates cognitive impairment in a murine model of Sepsis-associated encephalopathy by enhancing oligodendrocyte maturation and myelination in the mPFC YU2026 In a mouse model of sepsis-associated encephalopathy (SAE), mTOR hyperactivation impairs oligodendrocyte maturation and causes cognitive deficits; hydrogen gas and rapamycin suppress mTOR, restore myelination, and improve cognition in these mice. |
| 2026 | A | Aberrant excitatory neuronal ERBB4 promotes Alzheimer's disease pathology LEE2026 Ectopic ERBB4 in excitatory neurons is one of the earliest changes in AD mouse models and is necessary for synapse loss, reactive gliosis, amyloid plaque deposition and cognitive deficits in AD mice, and its overexpression in wild-type excitatory neurons is sufficient to reproduce synapse loss, gliosis and cognitive deficits (but not amyloid plaques); these effects require mTOR signalling downstream of ERBB4. |
| 2013 | A | mTORC2 controls actin polymerization required for consolidation of long-term memory HUA2013 Conditional deletion of Rictor in the postnatal mouse forebrain reduced mTORC2 activity and selectively impaired long-term memory and the late phase of hippocampal LTP, with a comparable long-term-memory deficit in dTORC2-deficient flies. Hippocampal actin polymerisation was reduced, and restoring it rescued both L-LTP and long-term memory; a compound that raised mTORC2 activity converted early LTP into late LTP and enhanced memory. This is the loss-of-function AND rescue evidence that mTORC2 is required for memory consolidation - the arm chronic rapamycin also disrupts, and the study Open Question H8 needs for its mTORC2 liability leg, which until 2026-09-05 rested on no supporting study at all. |
| 2012 | A | Chronic inhibition of mammalian target of rapamycin by rapamycin modulates cognitive and non-cognitive components of behavior throughout lifespan in mice. HAL2012 Asked whether the lifespan-extending dose of rapamycin harms or helps the aging BRAIN. Reassuringly, it enhanced learning and memory in young mice, prevented age-related cognitive decline in old ones, and even reduced anxiety and depression-like behavior - linked to boosted brain monoamines. Cognitive benefit, not cost. |
| 2009 | A | Pharmacological inhibition of mTORC1 suppresses anatomical, cellular, and behavioral abnormalities in neural-specific Pten knock-out mice ZHO2009 In neural Pten-knockout mice, rapamycin prevented and reversed neuronal hypertrophy and improved a subset of the PTEN-associated abnormal behaviours. |
| 2008 | A | Reversal of learning deficits in a Tsc2+/- mouse model of tuberous sclerosis EHN2008 Rapamycin reverses learning and memory deficits in a Tsc2+/- tuberous sclerosis model. |
Related entities
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