Article
Familial knockin mutation of LRRK2 causes lysosomal dysfunction and accumulation of endogenous insoluble α-synuclein in neurons.
Neurobiology of disease - 1 Mar 2018
Schapansky Jason, Khasnavis Saurabh, DeAndrade Mark P, Nardozzi Jonathan D, Falkson Samuel R, Boyd Justin D, Sanderson John B, Bartels Tim, Melrose Heather L, LaVoie Matthew J
Abstract excerpt
Missense mutations in the multi-domain kinase LRRK2 cause late onset familial Parkinson's disease. They most commonly with classic proteinopathy in the form of Lewy bodies and Lewy neurites comprised of insoluble α-synuclein, but in rare cases can also manifest tauopathy. The normal function of LRRK2 has remained elusive, as have the cellular consequences of its mutation. Data from LRRK2 null model organisms and...
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