Abstract
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.
Highlights
Neural stem cells (NSCs) are present in some areas of the adult brain that continue to produce new, functional neurons that are added to existing brain circuits
The process of adult neurogenesis is regulated, e.g. by environmental and hormonal factors like stress, growth factors, exercise and antidepressant drugs while alterations have been observed in neurodegenerative disorders [19], like epilepsy, stroke [20] or Alzheimer’s disease (AD), that suggested neurogenesis responds to these conditions [21]
Methylated DNA immunoprecipitation (MeDIP) analysis revealed that Gadd45b is necessary for demethylation at different genes encoding growth factors involved in neurogenesis, including FGF1 [81], which regulates self-renewal and proliferation of NSCs similar to fibroblast growth factor 2 (FGF2) [54]
Summary
Neural stem cells (NSCs) are present in some areas of the adult brain that continue to produce new, functional neurons that are added to existing brain circuits. It suggests that, in contrast to a role for MBD1 in early neurogenesis, MeCP2 binding to DNA methylation marks is important for regulating the expression of genes involved in maturation of newborn neurons.
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