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Journal Article

Tau protein is essential for stress-induced brain pathology

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Bedenk,  Benedikt
Max Planck Institute of Psychiatry, Max Planck Society;

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Mack,  Natalie
Max Planck Institute of Psychiatry, Max Planck Society;

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Czisch,  Michael
Max Planck Institute of Psychiatry, Max Planck Society;

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Almeida,  Osborne F. X.
Max Planck Institute of Psychiatry, Max Planck Society;

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Citation

Lopes, S., Vaz-Silva, J., Pinto, V., Dalla, C., Kokras, N., Bedenk, B., et al. (2016). Tau protein is essential for stress-induced brain pathology. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 113(26), E3755-E3763. doi:10.1073/pnas.1600953113.


Cite as: http://hdl.handle.net/11858/00-001M-0000-002C-E578-9
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 hyper-phosphorylation 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.