Gräff, Johannes2017-11-082017-11-082017-11-08201710.15252/embj.201798013https://infoscience.epfl.ch/handle/20.500.14299/142003WOS:000412115800001Epidemiological 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.text::journal::journal article::research article