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This phenomenon may be attributed to a reduced capacity of progenitor cells to replace oligodendrocytes probably due to an altered age-related expression of certain transcription factor such as Nkx2.2 (Doucette et al., 2010) or due to an inefficient age-dependent epigenetic modulation, as shown by a declined recruitment of histone deacetylases (HDACs) to promoter regions of oligodendrocyte differentiation inhibitors (Hes1, Hes5, Id2, and Id4) and neural stem cell markers such as Sox2 followed by insufficient deacytelation of nucleosomal histones and subsequent perturbances of myelin gene expression in older mice (Shen et al., 2008)

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Nicotinamide mononucleotide protects against - amyloid oligomer-induced cognitive impairment and neuronal death