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Defects in trafficking bridge Parkinson's disease pathology and genetics

Author

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  • Asa Abeliovich

    (Columbia University
    Columbia University
    Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University)

  • Aaron D. Gitler

    (Stanford University)

Abstract

Parkinson's disease is a debilitating, age-associated movement disorder. A central aspect of the pathophysiology of Parkinson's disease is the progressive demise of midbrain dopamine neurons and their axonal projections, but the underlying causes of this loss are unclear. Advances in genetics and experimental model systems have illuminated an important role for defects in intracellular transport pathways to lysosomes. The accumulation of altered proteins and damaged mitochondria, particularly at axon terminals, ultimately might overwhelm the capacity of intracellular disposal mechanisms. Cell-extrinsic mechanisms, including inflammation and prion-like spreading, are proposed to have both protective and deleterious functions in Parkinson's disease.

Suggested Citation

  • Asa Abeliovich & Aaron D. Gitler, 2016. "Defects in trafficking bridge Parkinson's disease pathology and genetics," Nature, Nature, vol. 539(7628), pages 207-216, November.
    • Handle: RePEc:nat:nature:v:539:y:2016:i:7628:d:10.1038_nature20414
    DOI: 10.1038/nature20414
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    Cited by:

    1. Wang, Zhizhi & Hu, Bing & Zhou, Weiting & Xu, Minbo & Wang, Dingjiang, 2023. "Hopf bifurcation mechanism analysis in an improved cortex-basal ganglia network with distributed delays: An application to Parkinson’s disease," Chaos, Solitons & Fractals, Elsevier, vol. 166(C).

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