Journal
NATURE REVIEWS NEUROSCIENCE
Volume 17, Issue 4, Pages 251-260Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nrn.2016.13
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Funding
- NIA NIH HHS [AG046275, P01 AG015379, RF1 AG006173, R01 AG006173, R21 AG047505, R37 AG006173, R01 AG046275, AG047505, AG06173] Funding Source: Medline
- NINDS NIH HHS [R01 NS083845, NS083845] Funding Source: Medline
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There has been an explosion in the number of papers discussing the hypothesis of 'pathogenic spread' in neurodegenerative disease - the idea that abnormal forms of disease-associated proteins, such as tau or a-synuclein, physically move from neuron to neuron to induce disease progression. However, whether inter-neuronal spread of protein aggregates actually occurs in humans and, if so, whether it causes symptom onset remain uncertain. Even if pathogenic spread is proven in humans, it is unclear how much this would alter the specific therapeutic approaches that are in development. A critical appraisal of this increasingly popular hypothesis thus seems both important and timely.
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