Journal
COLD SPRING HARBOR PERSPECTIVES IN BIOLOGY
Volume 8, Issue 11, Pages -Publisher
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/cshperspect.a023630
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Funding
- German Research Council (Deutsche Forschungsgemeinschaft [DFG]) [TR 1000/1-1]
- Michael J. Fox Foundation for Parkinson's Disease Research
- Annemarie Opprecht Prize (Bern, Switzerland)
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Experimental data indicate that transneuronal propagation of abnormal protein aggregates in neurodegenerative proteinopathies, such as sporadic Alzheimer's disease (AD) and Parkinson's disease (PD), is capable of a self-propagating process that leads to a progression of neurodegeneration and accumulation of prion-like particles. The mechanisms by which misfolded tau and alpha-synuclein possibly spread from one involved nerve cell to the next in the neuronal chain to induce abnormal aggregation are still unknown. Based on findings from studies of human autopsy cases, we review potential pathways and mechanisms related to axonal and transneuronal dissemination of tau (sporadic AD) and alpha-synuclein (sporadic PD) aggregates between anatomically interconnected regions.
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