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.
Enrico Amico, Antonella Romano
Jian Wang, Friedhelm Christoph Hummel
Susanne Johanna Petronella Léonie Vissers