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Article

Mutant LRRK2 toxicity in neurons depends on LRRK2 levels and synuclein but not kinase activity or inclusion bodies.

The Journal of neuroscience : the official journal of the Society for Neuroscience - 8 Jan 2014

Skibinski Gaia, Nakamura Ken, Cookson Mark R, Finkbeiner Steven

Abstract excerpt

By combining experimental neuron models and mathematical tools, we developed a "systems" approach to deconvolve cellular mechanisms of neurodegeneration underlying the most common known cause of Parkinson's disease (PD), mutations in leucine-rich repeat kinase 2 (LRRK2). Neurons ectopically expressing mutant LRRK2 formed inclusion bodies (IBs), retracted neurites, accumulated synuclein, and died prematurely,...

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Source

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Identifiers

PMID: 24403142
DOI: 10.1523/JNEUROSCI.2712-13.2014
PMCID: PMC3870929

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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