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Proc Natl Acad Sci U S A. 2016 Jun 28;113(26):E3755-63. doi: 10.1073/pnas.1600953113. Epub 2016 Jun 6.

Tau protein is essential for stress-induced brain pathology.

Author information

1
Life and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho, 4710-057 Braga, Portugal; ICVS/3B's-PT Government Associate Laboratory, 4710-057 Braga/Guimarães, Portugal;
2
Department of Pharmacology, Medical School of Athens, 11527 Goudi, Greece;
3
Max Planck Institute of Psychiatry, 80804 Munich, Germany.
4
Life and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho, 4710-057 Braga, Portugal; ICVS/3B's-PT Government Associate Laboratory, 4710-057 Braga/Guimarães, Portugal; ioannis@ecsaude.uminho.pt.

Abstract

Exposure to chronic stress is frequently accompanied by cognitive and affective disorders in association with neurostructural adaptations. Chronic stress was previously shown to trigger Alzheimer's-like neuropathology, which is characterized by Tau hyperphosphorylation and missorting into dendritic spines followed by memory deficits. Here, we demonstrate that stress-driven hippocampal deficits in wild-type mice are accompanied by synaptic missorting of Tau and enhanced Fyn/GluN2B-driven synaptic signaling. In contrast, mice lacking Tau [Tau knockout (Tau-KO) mice] do not exhibit stress-induced pathological behaviors and atrophy of hippocampal dendrites or deficits of hippocampal connectivity. These findings implicate Tau as an essential mediator of the adverse effects of stress on brain structure and function.

KEYWORDS:

Tau; depression; hippocampus; memory deficits; stress

PMID:
27274066
PMCID:
PMC4932951
DOI:
10.1073/pnas.1600953113
[Indexed for MEDLINE]
Free PMC Article

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