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Defects in trafficking bridge Parkinson's disease pathology and genetics
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Journal Article
Defects in trafficking bridge Parkinson's disease pathology and genetics
2016
Overview
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.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ 631/378
/ 631/80
/ 692/699
/ alpha-Synuclein - metabolism
/ Animals
/ Biological Transport - genetics
/ Dopamine
/ Genes
/ Genetics
/ Genomes
/ Glucosylceramidase - genetics
/ Glucosylceramidase - metabolism
/ Humanities and Social Sciences
/ Humans
/ Kinases
/ Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 - genetics
/ Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 - metabolism
/ Mutation
/ Neurons
/ Parkinson Disease - genetics
/ Parkinson Disease - metabolism
/ Parkinson Disease - pathology
/ Proteins
/ Science
