Helen S. Bateup
Senior/corresponding author of a 2026 Nature study showing mTORC1 hyperactivity drives cell-autonomous astrocyte reactivity in tuberous sclerosis
Associate Professor of Molecular and Cell Biology & Neuroscience, University of California, Berkeley · Weill Neurohub Investigator · PhD, The Rockefeller University
Helen Bateup directs a lab in UC Berkeley's Department of Molecular and Cell Biology studying how genetic mutations linked to epilepsy and autism — especially in the TSC1/TSC2–mTORC1 pathway — disrupt neural development, synaptic function and circuit excitability. She trained as a PhD student at The Rockefeller University and is a Weill Neurohub Investigator.
In this Atlas she is senior/corresponding author of a 2026 Nature study using human brain organoids grown for 9+ months (to replicate human developmental timelines) alongside resected tuber tissue from tuberous sclerosis patients. The work shows that TSC2 loss biases neural progenitors toward reactive, pro-inflammatory astrocytes in a cell-autonomous manner — independent of seizures — implicating glial dysfunction, not just neuronal hyperexcitability, as a driver of TSC pathology and a potential therapeutic target.
Milestones in the Atlas
| Year | Evidence | Study |
|---|---|---|
| 2026 | M | mTORC1 drives cell-autonomous astrocyte reactivity in tuberous sclerosis LI2026C Senior/corresponding author demonstrating that mTORC1-hyperactive neural progenitors become pro-inflammatory reactive astrocytes in a cell-autonomous manner, independent of seizure activity — implicating glial dysfunction as a driver, not only a consequence, of TSC pathology. |
Co-authors in the Atlas
People with a profile here who share at least one study with Helen S. Bateup.
- Thomas L. Li Co-first author of a 2026 Nature study showing mTORC1 hyperactivity drives reactive astrocytes as a primary, seizure-independent consequence of TSC2 loss, implicating glial dysfunction as a driver of tuberous sclerosis pathology