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Formin 2 links neuropsychiatric phenotypes at young age to an increased risk for dementia
RC. Agís-Balboa, PS. Pinheiro, N. Rebola, C. Kerimoglu, E. Benito, M. Gertig, S. Bahari-Javan, G. Jain, S. Burkhardt, I. Delalle, A. Jatzko, M. Dettenhofer, PA. Zunszain, A. Schmitt, P. Falkai, JC. Pape, EB. Binder, C. Mulle, A. Fischer, F. Sananbenesi,
Jazyk angličtina Země Velká Británie
Typ dokumentu časopisecké články, práce podpořená grantem
NLK
Free Medical Journals
od 1982 do Před 1 rokem
PubMed Central
od 1982
Europe PubMed Central
od 1982 do Před 1 rokem
Open Access Digital Library
od 1997-01-01
Open Access Digital Library
od 1997-01-01
Medline Complete (EBSCOhost)
od 1997-01-02 do Před 1 rokem
Wiley Free Content
od 1997 do Před 1 rokem
PubMed
28768717
DOI
10.15252/embj.201796821
Knihovny.cz E-zdroje
- MeSH
- demence epidemiologie genetika psychologie MeSH
- dospělí MeSH
- fenotyp MeSH
- jaderné proteiny genetika MeSH
- lidé středního věku MeSH
- lidé MeSH
- mikrofilamentové proteiny genetika MeSH
- myši knockoutované MeSH
- myši MeSH
- neuroplasticita genetika MeSH
- paměť fyziologie MeSH
- posttraumatická stresová porucha komplikace epidemiologie genetika MeSH
- rizikové faktory MeSH
- stárnutí genetika fyziologie MeSH
- studie případů a kontrol MeSH
- věk při počátku nemoci MeSH
- zvířata MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
Age-associated memory decline is due to variable combinations of genetic and environmental risk factors. How these risk factors interact to drive disease onset is currently unknown. Here we begin to elucidate the mechanisms by which post-traumatic stress disorder (PTSD) at a young age contributes to an increased risk to develop dementia at old age. We show that the actin nucleator Formin 2 (Fmn2) is deregulated in PTSD and in Alzheimer's disease (AD) patients. Young mice lacking the Fmn2 gene exhibit PTSD-like phenotypes and corresponding impairments of synaptic plasticity, while the consolidation of new memories is unaffected. However, Fmn2 mutant mice develop accelerated age-associated memory decline that is further increased in the presence of additional risk factors and is mechanistically linked to a loss of transcriptional homeostasis. In conclusion, our data present a new approach to explore the connection between AD risk factors across life span and provide mechanistic insight to the processes by which neuropsychiatric diseases at a young age affect the risk for developing dementia.
CEITEC Central European Institute of Technology Masaryk University Brno Czech Republic
Department of Pathology and Laboratory Medicine Boston University School of Medicine Boston MA USA
Department of Psychiatry and Psychotherapy LMU Munich Munich Germany
Department of Psychiatry and Psychotherapy University Medical Center Göttingen Göttingen Germany
Department of Translational Research in Psychiatry Max Planck Institute of Psychiatry Munich Germany
Citace poskytuje Crossref.org
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- $a Agís-Balboa, Roberto Carlos $u Department for Epigenetics and Systems Medicine in Neurodegenerative Diseases, German Center for Neurodegenerative Diseases (DZNE) Göttingen, Göttingen, Germany.
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