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Epigenetic regulation of adult neural stem cells: implications for Alzheimer’s disease

Experimental evidence has demonstrated that several aspects of adult neural stem cells (NSCs), including their quiescence, proliferation, fate specification and differentiation, are regulated by epigenetic mechanisms. These control the expression of specific sets of genes, often including those enco...

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Detalles Bibliográficos
Autores principales: Fitzsimons, Carlos P, van Bodegraven, Emma, Schouten, Marijn, Lardenoije, Roy, Kompotis, Konstantinos, Kenis, Gunter, van den Hurk, Mark, Boks, Marco P, Biojone, Caroline, Joca, Samia, Steinbusch, Harry WM, Lunnon, Katie, Mastroeni, Diego F, Mill, Jonathan, Lucassen, Paul J, Coleman, Paul D, van den Hove, Daniel LA, Rutten, Bart PF
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4080757/
https://www.ncbi.nlm.nih.gov/pubmed/24964731
http://dx.doi.org/10.1186/1750-1326-9-25
Descripción
Sumario:Experimental evidence has demonstrated that several aspects of adult neural stem cells (NSCs), including their quiescence, proliferation, fate specification and differentiation, are regulated by epigenetic mechanisms. These control the expression of specific sets of genes, often including those encoding for small non-coding RNAs, indicating a complex interplay between various epigenetic factors and cellular functions. Previous studies had indicated that in addition to the neuropathology in Alzheimer’s disease (AD), plasticity-related changes are observed in brain areas with ongoing neurogenesis, like the hippocampus and subventricular zone. Given the role of stem cells e.g. in hippocampal functions like cognition, and given their potential for brain repair, we here review the epigenetic mechanisms relevant for NSCs and AD etiology. Understanding the molecular mechanisms involved in the epigenetic regulation of adult NSCs will advance our knowledge on the role of adult neurogenesis in degeneration and possibly regeneration in the AD brain.