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Epidemiological evidence suggests that people suffering from post-traumatic stress disorder have a higher risk for developing Alzheimer's disease. The underlying mechanisms, however, remained thus far unexplored. In this issue of The EMBO Journal, Agis-Balboa etal (2017) show that the actin-associated protein Formin 2 is reduced in both conditions and that its downregulation in mice accelerates Alzheimer-related pathophysiology via aberrant epigenetic and transcriptional changes. Treating mice with a histone deacetylase inhibitor (HDACi) delayed Alzheimer-related pathologies, lending experimental support to ongoing clinical trials with HDACis against traumatic memories and Alzheimer's disease.
Type
research article
Web of Science ID
WOS:000412115800001
Authors
Publication date
2017
Publisher
Published in
Volume
36
Issue
19
Start page
2809
End page
2811
Peer reviewed
REVIEWED
EPFL units
Available on Infoscience
November 8, 2017
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