Kaitlyn M. L. Cramb

The paper investigates dopamine release defects in Parkinson's patient-derived neurons and identifies reduced VMAT2 function as the cause.

This study shows that SARM1 activation causes mitochondrial dysfunction in human neurons, which can be reversed by nicotinamide or prevented by antisense oligonucleotides.

The paper identifies Anxa1+ dopamine neurons as vulnerable in prodromal Parkinson's disease, linking their dysfunction to bradykinesia and procedural motor learning impairments.

This study shows that the GBA-N370S mutation causes early hyperexcitability in striatal neurons by reducing sodium and potassium currents, which can be mitigated by aging or PKA antagonism.