Darren J. Moore

This study shows that neuroinflammation occurs early in a mouse model of prodromal Parkinson's disease before neuronal loss, linking Syn pathology to olfactory dysfunction.

This study identifies a selective effect of the D620N VPS35 mutation on the brain-specific protein interactome in mammalian cells and brain tissue.

The paper investigates how G2019S LRRK2 interacts with metabolic syndrome in a mouse model of Parkinson's disease, showing systemic nucleotide and energy metabolism disruptions and mitochondrial dysfunction.

This paper investigates how LRRK2 phosphorylates ArfGAP1, affecting its localization, activity, and toxicity in neurons, with implications for Parkinson's disease.

This study evaluates how LRRK2 coding variants affect protein function and neurotoxicity, finding that G2385R increases Rab10 phosphorylation and impairs neuronal integrity.

This study shows that pathological α-synuclein can cause granulovacuolar degeneration independently of tau, using a mouse model of α-synucleinopathy.

This study shows that α-synuclein pathology spreads independently of ATP13A2 in a mouse model, indicating ATP13A2 is not critical for -syn clearance or propagation.

This study shows that deleting ATP13A2 in adult mice leads to progressive dopaminergic degeneration and lysosomal issues, mimicking human neurodegenerative diseases.

The paper measures LRRK2 kinase activity via pT73-Rab10 in serum, linking it to inflammation and Parkinson's disease severity.

This study shows that LRRK2 does not significantly affect the formation of α-synuclein inclusions in the forebrain of mice after PFF injection, but may influence microglial activation.

This study shows that α-synuclein fibrils injected into mouse forebrain cause regional pathology, early neuronal degeneration, and cognitive deficits resembling Lewy body diseases.

This study investigates the interaction between VPS35 and α-synuclein in PD models and finds no significant functional or pathological interaction.

The paper investigates how lifespan-extending genetic pathways provide neuroprotection in a nematode model of Parkinson's disease, showing dissociation between lifespan extension and neuroprotection.

This study develops a rat model of Parkinson's disease caused by the G2019S LRRK2 mutation and shows that kinase and GTPase activities are critical for neurodegeneration.