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Spreading of tau pathology in A lzheimer's disease by cell‐to‐cell transmission
Author(s) -
Mohamed NguyenVi,
Herrou Thibaut,
Plouffe Vanessa,
Piperno Nicolas,
Leclerc Nicole
Publication year - 2013
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/ejn.12229
Subject(s) - neuroscience , entorhinal cortex , tau pathology , postsynaptic potential , extracellular , genetically modified mouse , biology , secretion , microbiology and biotechnology , neurodegeneration , neurotransmission , cell , transgene , hippocampal formation , alzheimer's disease , pathology , disease , receptor , medicine , biochemistry , gene
It is well documented that neurofibrillary tangles composed of aggregated tau protein propagate in a predictable pattern in A lzheimer's disease ( AD ). The mechanisms underlying the propagation of tau pathology are still poorly understood. Recent studies have provided solid data demonstrating that in several neurodegenerative diseases including AD , the spreading of misfolded protein aggregates in the brain would result from prion‐like cell‐to‐cell transmission. Consistent with this new concept, recent studies have reported that human tau can be released in the extracellular space by an active process of secretion, and can be endocytosed both in vitro and in vivo . Most importantly, it was reported that the spreading of tau pathology was observed along synaptically connected circuits in a transgenic mouse model where human tau overexpression was restricted in the entorhinal cortex. This indicates that secretion of tau by presynaptic neurons and its uptake by postsynaptic neurons could be the sequential events leading to the propagation of tau pathology in the brain.