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
Department of Molecular and Cell Biology & Department of Neuroscience, University of California, Berkeley
Thomas L. Li is a researcher in the Department of Molecular and Cell Biology and the Department of Neuroscience at UC Berkeley. No further public biographical details were found.
In this Atlas he is co-first author of a 2026 Nature study, from Helen Bateup's lab, using human brain organoids carrying TSC2 mutations plus patient-derived cortical tuber tissue to show that hyperactive mTORC1 signaling biases neural progenitors toward becoming enlarged, pro-inflammatory reactive astrocytes — independent of seizure activity — implicating glial dysfunction as a driver of tuberous sclerosis pathology rather than only a downstream consequence of seizures.
Milestones in the Atlas
| Year | Evidence | Study |
|---|---|---|
| 2026 | M | mTORC1 drives cell-autonomous astrocyte reactivity in tuberous sclerosis LI2026C Co-first author using human brain organoids and patient tuber tissue to show that TSC2 loss drives neural progenitors into reactive, pro-inflammatory astrocytes independent of seizures. |
Co-authors in the Atlas
People with a profile here who share at least one study with Thomas L. Li.
- Helen S. Bateup Senior/corresponding author of a 2026 Nature study showing mTORC1 hyperactivity drives cell-autonomous astrocyte reactivity in tuberous sclerosis