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Cold Spring Harb Perspect Biol. 2016 Nov 1;8(11). pii: a023630. doi: 10.1101/cshperspect.a023630.

Potential Pathways of Abnormal Tau and α-Synuclein Dissemination in Sporadic Alzheimer's and Parkinson's Diseases.

Author information

1
Clinical Neuroanatomy Section/Department of Neurology, Center for Biomedical Research, University of Ulm, Helmholtzstrasse 8/1, 89081 Ulm, Germany.

Abstract

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 α-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 α-synuclein (sporadic PD) aggregates between anatomically interconnected regions.

PMID:
27580631
PMCID:
PMC5088528
DOI:
10.1101/cshperspect.a023630
[Indexed for MEDLINE]
Free PMC Article

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