Neelam Shahani

This study identifies Dipyridamole as a drug that rescues mitochondrial dysfunction and neuronal death in ALS and AD iPSC-derived neurons by enhancing mitochondrial pyruvate uptake.

This study identifies nuclear GAPDH translocation as a mediator of stress-induced cardiac hypertrophy through BRG1-associated chromatin remodeling in mice and human patients.

This study shows Rhes moves between neurons and transports mutant huntingtin in the brain, with Rhes deletion reducing this transport.

This study shows that Rhes deletion reduces age-dependent motor deficits and mTORC1-S6K hyperphosphorylation in a mouse model of Huntington disease.

This study shows that deleting SUMO1 in HD mice reduces motor and neurological impairments by enhancing autophagy and reducing mHTT levels.

The paper uses ribosome profiling to show that mitochondrial-encoded OXPHOS mRNA translation is increased while nuclear-encoded OXPHOS mRNA translation is decreased in Huntington disease striatal cells.

This study shows that mTORC1 in the striatum prevents haloperidol-induced catalepsy, suggesting it could be a target for reducing antipsychotic side effects.

This study identifies cGAS as a key DNA sensor upregulated in Huntington disease, promoting inflammation and autophagy through increased mRNA occupancy and protein activity.

This study identifies Rhes as a striatal-enriched protein that promotes mitophagy via Nix, contributing to striatal vulnerability in the brain.

This study identifies RasGRP1 as a key mediator of L-DOPA-induced dyskinesia in a mouse model of Parkinson's disease, showing its role in multiple signaling pathways and potential as a therapeutic target.

This study shows mutant huntingtin (mHtt) stalls ribosomes and suppresses protein synthesis independently of FMRP, using ribosome profiling in HD cells and mouse models.