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Article

Deficiency of ATP13A2 leads to lysosomal dysfunction, α-synuclein accumulation, and neurotoxicity.

The Journal of neuroscience : the official journal of the Society for Neuroscience - 21 Mar 2012

Usenovic Marija, Tresse Emilie, Mazzulli Joseph R, Taylor J Paul, Krainc Dimitri

Abstract excerpt

The autophagy-lysosomal pathway plays an important role in the clearance of long-lived proteins and dysfunctional organelles. Lysosomal dysfunction has been implicated in several neurodegenerative disorders including Parkinson's disease and related synucleinopathies that are characterized by accumulations of α-synuclein in Lewy bodies. Recent identification of mutations in genes linked to lysosomal function and...

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Source

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Identifiers

PMID: 22442086
DOI: 10.1523/JNEUROSCI.5575-11.2012
PMCID: PMC3462811

Genes

ATP13A2

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

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Deficiency of ATP13A2 leads to lysosomal dysfunction, α-synuclein accumulation, and neurotoxicity.PMID 22442086Read ↗

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Loss of P-type ATPase ATP13A2/PARK9 function induces general lysosomal deficiency and leads to Parkinson disease neurodegenerationSemantic proximity Read ↗

Identification of novel ATP13A2 interactors and their role in α-synuclein misfolding and toxicitySemantic proximity Read ↗

Atp13a2-deficient mice exhibit neuronal ceroid lipofuscinosis, limited α-synuclein accumulation and age-dependent sensorimotor deficitsSemantic proximity Read ↗

The Roles of ATP13A2 Gene Mutations Leading to Abnormal Aggregation of α-Synuclein in Parkinson’s DiseaseSemantic proximity Read ↗

Pathogenic effects of novel mutations in the P-type ATPase ATP13A2 (PARK9) causing Kufor-Rakeb syndrome, a form of early-onset parkinsonism.Semantic proximity Read ↗

Hereditary parkinsonism with dementia is caused by mutations in ATP13A2, encoding a lysosomal type 5 P-type ATPase.Semantic proximity Read ↗

α-Synuclein-Independent Histopathological and Motor Deficits in Mice Lacking the Endolysosomal Parkinsonism Protein Atp13a2Semantic proximity Read ↗

Mutation of the parkinsonism gene ATP13A2 causes neuronal ceroid-lipofuscinosis.Semantic proximity Read ↗

Common Pathogenic Effects of Missense Mutations in the P-Type ATPase ATP13A2 (PARK9) Associated with Early-Onset ParkinsonismSemantic proximity Read ↗

Pathogenic LRRK2 mutations, through increased kinase activity, produce enlarged lysosomes with reduced degradative capacity and increase ATP13A2 expression.Semantic proximity Read ↗

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