Ayşe Ulusoy

This study shows that α-synuclein accumulation in dopaminergic neurons leads to mitochondrial dysfunction and changes in circadian gene expression, contributing to neuronal damage in Parkinson's disease.

This study uses spatial transcriptomics to show that ALDH1A1+ and ALDH1A1- midbrain dopaminergic neurons respond differently to alpha-synuclein overexpression, with distinct transcriptional changes over time.

This study shows that targeting nitrated alpha-synuclein with an antibody reduces pathology in Parkinson's disease models and correlates with increased levels in Parkinson's patients.

This study shows that GBA1 mutations increase mitochondrial oxidative stress, leading to alpha-synuclein aggregation and spreading in a mouse model of Parkinson's disease.

This study shows that nitration of alpha-synuclein after fibrillization reduces its seeding activity and pathology formation in neurons and in vivo.

This study identifies BCL11A as a defining transcription factor for a distinct subset of midbrain dopamine neurons, showing their vulnerability to Parkinson's disease and developmental roles in motor function.

The paper simulates alpha-synuclein spread using a connectome model and finds connectivity alone is insufficient to explain observed pathology patterns in rats.