DNA Damage and Repair in Central Nervous System Injury Biology Diagrams Accumulation of DNA damage has been observed in human and mouse HSCs as well as in muscle, intestinal, mesenchymal, neural, skin and germ stem cells 72. Accumulation of DNA damage may be particularly prevalent in the central nervous system owing to the low DNA repair capacity in postmitotic brain tissue. It is generally believed that the cumulative effects of the deleterious changes that occur in aging, mostly after the reproductive phase, contribute to species-specific rates of aging.
The accumulation of these DNA damage can be particularly deleterious in postmitotic cells such as neurons, which are not self-renewed through cell proliferation (Coppede and Migliore 2009). It is believed that DNA damage can promote the age-associated neurodegenerative process such as Alzheimer's disease Many factors contribute to aging, such as the time-dependent accumulation of macromolecular damage, including DNA damage. The integrity of the nuclear genome is essential for cellular, tissue, and organismal health. DNA damage is a constant threat because nucleic acids are chemically unstable under physiological conditions and vulnerable to It is thought that DNA damage accumulation with aging results in loss of cellular functionality and ultimately degeneration of cells and tissues. Erroneous repair, however, can lead to mutations and chromosomal aberrations, which when affecting tumor suppressor genes, drive carcinogenesis. Alternatively, unrepaired DNA lesions can lead to cell
The central role of DNA damage in the ageing process Biology Diagrams
The accumulation of DNA double-strand damage has been observed in aging mice and human cells (Sedelnikova et al., 2004a).In AD model mice, it has been observed that exploring new environments leads to increased DNA double-strand damage in several brain regions, especially those involved in spatial learning and memory pairs (Suberbielle et al., 2013), and elevated levels of ฮณ-H2AX in Recent studies have highlighted the role of DNA damage, particularly DNA double-strand breaks (DSBs), in the progression of neuronal loss in a broad spectrum of neurodegenerative diseases. In the present study, we tested the hypothesis that accumulation of DNA DSB plays an important role in AD pathogenesis. Overall, these lines of evidence suggest DNA damage accumulation in aged skin stem cells and raises the question of how these stem cells address this burden. HFSCs, as many of the tissue specific stem cells, are more resistant to DNA damage induced apoptosis compared to more differentiated cells (Solanas et al. 2017; Gutierrez-Martinez et al. 2018
