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Nature. 2016 Nov 10;539(7628):207-216. doi: 10.1038/nature20414.

Defects in trafficking bridge Parkinson's disease pathology and genetics.

Author information

1
Department of Pathology and Cell Biology, Columbia University, New York, New York 10032, USA.
2
Department of Neurology, Columbia University, New York, New York 10032, USA.
3
Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University, New York, New York 10032, USA.
4
Department of Genetics, Stanford University, Stanford, California 94305, USA.

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.

PMID:
27830778
DOI:
10.1038/nature20414
[Indexed for MEDLINE]

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