Donato A. Di Monte

TL;DR: Overexpression of human α‐synuclein in the lower brainstem is sufficient to induce its long‐distance caudo‐rostral propagation, recapitulating features of Parkinson's disease and mechanisms of disease progression.

TL;DR: It is demonstrated in vivo that repeated systemic challenge of mice over four consecutive days with bacterial LPS maintained an elevated microglial inflammatory phenotype and induced loss of dopaminergic neurons in the substantia nigra, confirming the involvement of the complement system in neurodegeneration.

TL;DR: Results of this in vivo study revealed a route-specific transmission of α-synuclein from the rat brain to the stomach, and the dorsal motor nucleus of the vagus nerve represents a key relay center for central-to-peripheral α- synuclein transmission, and efferent vagal fibers may act as unique conduits for protein transfer.

TL;DR: It is hypothesized that ASYN may act physiologically as a catalytically regenerated scavenger of oxidants in healthy cells, thus performing an important protective role prior to the onset of disease or during aging.

TL;DR: It is demonstrated in cell culture, nematode, and rodent models of PD that leucine-rich repeat kinase 2 (LRRK2), a PD-linked kinase, modulates α-synuclein propagation in a kinase activity-dependent manner and that this is dependent on phosphorylation of one of its substrates, RAB35.