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Project

Investigation of the role of the lysosomal P-type ATPases ATP13A2 and ATP10B in preclinical models for Parkinson’s disease

Parkinson’s disease (PD) is the second most common neurodegenerative disorder with no current disease modifying therapy available. While several molecular mechanisms are implicated in PD, such as alpha-synuclein aggregation and mitochondrial dysfunction, accumulating evidence puts lysosomal dysfunction at the center stage of PD pathogenesis. Recent evidence has implicated two lysosomal ATPases, ATP13A2 and ATP10B in early onset PD and related disorders. Loss of ATP10B and ATP13A2 leads to lysosomal accumulation of substrates such as spermine and glucosylceramide (GluCer), leading to lysosomal rupture and mitochondrial dysfunction. In this project we want to further increase our knowledge on the pathogenic role of ATP13A2 and ATP10B in preclinical models for PD and preclinically validate ATP13A2 and/or ATP10B activation as therapeutic approach(es).

Date:17 Dec 2020 →  Today
Keywords:Neurodegeneration, Viral vectors, Parkinson Disease
Disciplines:Behavioural neuroscience
Project type:PhD project