@article {38970,
	title = {Tau protein is essential for stress-induced brain pathology},
	journal = {Proc Natl Acad Sci U S A},
	volume = {113},
	number = {26},
	year = {2016},
	note = {10.1073/pnas.1600953113},
	month = {Jun 28},
	pages = {E3755-63},
	edition = {20160606},
	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{\textquoteright}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 = {Adaptor Proteins, Signal Transducing/genetics/metabolism, Alzheimer Disease/genetics/*metabolism/pathology/physiopathology, Animals, Brain/metabolism/pathology, Dendritic Spines/metabolism, Depression, Disease Models, Animal, Hippocampus, Hippocampus/*metabolism/pathology, Humans, Male, Memory, memory deficits, Mice, Mice, Inbred C57BL, Mice, Knockout, Phosphorylation, stress, Stress, Physiological, Synapses/metabolism, Tau, tau Proteins/genetics/*metabolism},
	isbn = {0027-8424 (Print)0027-8424},
	author = {Lopes, S. and Vaz-Silva, J. and Pinto, V. and Dalla, C and Kokras, N and Bedenk, B. and Mack, N. and Czisch, M. and Almeida, O. F. and Sousa, N. and Sotiropoulos, I}
}
