Journal
JOURNAL OF NEUROSCIENCE
Volume 37, Issue 41, Pages 9799-9807Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.1787-16.2017
Keywords
aging; alpha-synuclein; calcium; mitochondria; neurodegeneration; neuron; selective vulnerability; synapse
Categories
Funding
- National Institutes of Health [NS047085]
- JPB Foundation
- IDP Foundation
- National Health and Medical Research Council [1079679]
- Plan Nacional, Ministerio de Economia y Competitividad [SAF2012-40216, SAF 2015-67239-P]
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The notion that prion-like spreading of misfolded alpha-synuclein (alpha-SYN) causes Parkinson's disease (PD) has received a great deal of attention. Although attractive in its simplicity, the hypothesis is difficult to reconcile with postmortem analysis of human brains and connectome-mapping studies. An alternative hypothesis is that PD pathology is governed by regional or cell-autonomous factors. Although these factors provide an explanation for the pattern of neuronal loss in PD, they do not readily explain the apparently staged distribution of Lewy pathology in many PD brains, the feature of the disease that initially motivated the spreading hypothesis by Braak and colleagues. While each hypothesis alone has its shortcomings, a synthesis of the two can explain much of what we know about the etiopathology of PD.
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