Hebrew University finds nitric oxide autism link
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- Hebrew University of Jerusalem researchers uncovered a molecular chain reaction where nitric oxide modifies TSC2, leading to overactive mTOR signaling in autism models.
- Prof. Haitham Amal led the study, which was published in Molecular Psychiatry, a Nature publishing group journal.
- Shashank Ojha and his team showed that lowering nitric oxide production prevented TSC2 S‑nitrosylation and restored normal mTOR activity in experimental neurons.
- Dr. Adi Aran recruited clinical samples from children with SHANK3 mutations and idiopathic ASD, which displayed reduced TSC2 and heightened mTOR signaling, mirroring lab results.
- Molecular Psychiatry published the paper (authors: Shashank Kumar Ojha, Maryam Kartawy, etc.) linking nitric‑oxide‑mediated S‑nitrosylation of TSC2 to mTOR dysregulation across autism models.
- Nitric oxide can S‑nitrosylate TSC2, marking it for degradation and weakening the brake on mTOR, as shown in neuronal cultures.
- TSC2 functions as a brake on mTOR; its loss due to nitric‑oxide‑induced modification drives overactive mTOR signaling that may disrupt neuronal communication.
Why it matters: The discovery gives autism researchers a concrete molecular target—nitric‑oxide‑driven TSC2 S‑nitrosylation—to modulate mTOR activity, opening a pathway for drug development. It also validates mTOR over‑activation across genetic and idiopathic ASD, meaning therapies that restore TSC2 function could benefit a broader patient cohort.
