Donato A. Di Monte

α-Synuclein impairs mitochondrial function and alters cryptochrome regulation in the substantia nigra

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.

Spatiotemporal transcriptomics reveals distinct responses of ALDH1A1-positive and ALDH1A1-negative midbrain dopaminergic neurons to alpha-synuclein overexpression

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.

Antibody treatment targeting nitrated alpha-synuclein counteracts protein spreading pathology

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.

Metabolic reprogramming and altered ATP content impair neuroprotective functions of microglia in β-glucocerebrosidase deficiency models

This study shows that GCase deficiency in microglia leads to metabolic changes and ATP depletion, impairing their neuroprotective functions and increasing neuronal vulnerability in Parkinson's disease.

Mitochondrial oxidant stress promotes alpha-synuclein aggregation and spreading in mice with mutated glucocerebrosidase

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.

Post-fibrillization nitration of alpha-synuclein abolishes its seeding activity and pathology formation in primary neurons and in vivo

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

The proSAAS chaperone provides neuroprotection and attenuates transsynaptic α-synuclein spread in rodent models of Parkinson's disease

This paper demonstrates that proSAAS overexpression protects dopaminergic neurons and reduces transsynaptic α-synuclein spread in Parkinson's disease models.

Inhibition of microglial GBA hampers the microglia-mediated anti-oxidant and protective response in neurons

This study shows that inhibiting microglial GBA reduces their ability to support neuronal antioxidant responses, increasing neuronal vulnerability to toxins.

The transcription factor BCL11A defines a distinctive subset of dopamine neurons in the developing and adult midbrain

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 connectome is necessary but not sufficient for the spread of alpha-synuclein pathology in rats

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