2022
DOI: 10.3390/ijms23094653
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DNA Double-Strand Breaks as Pathogenic Lesions in Neurological Disorders

Abstract: The damage and repair of DNA is a continuous process required to maintain genomic integrity. DNA double-strand breaks (DSBs) are the most lethal type of DNA damage and require timely repair by dedicated machinery. DSB repair is uniquely important to nondividing, post-mitotic cells of the central nervous system (CNS). These long-lived cells must rely on the intact genome for a lifetime while maintaining high metabolic activity. When these mechanisms fail, the loss of certain neuronal populations upset delicate … Show more

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Cited by 19 publications
(14 citation statements)
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“…Genomic damage during AD involves iron-derived oxidants. Heme from microbleeds and microhemorrhages may contribute to oxidants via iron from heme degradation by heme oxygenases 81 . AD brains have 2-fold increased double-strand DNA breaks (DSB) in neurons and astrocytes 82 .…”
Section: Discussionmentioning
confidence: 99%
“…Genomic damage during AD involves iron-derived oxidants. Heme from microbleeds and microhemorrhages may contribute to oxidants via iron from heme degradation by heme oxygenases 81 . AD brains have 2-fold increased double-strand DNA breaks (DSB) in neurons and astrocytes 82 .…”
Section: Discussionmentioning
confidence: 99%
“…DNA double-strand breaks (DSBs) are one of the most cytotoxic lesions caused by endogenous damaging events such as replication stress, reactive oxygen species, and exogenous agents such as ionizing radiation (IR) and chemical agents. If not repaired or improperly repaired, the damaged DNA can cause abnormalities in cellular functions and disease progression. , The DSBs occurring in the G2 phase of the cell cycle are mainly repaired by the error-free, homologous recombination (HR)-mediated repair pathway. , The HR repair is initiated with 3′-end resection, generating single-stranded DNA (ssDNA) overhangs . In eukaryotic cells, the ssDNA binding protein (SSB) complexes, e.g., RPA, the sensor of single-stranded DNA complex 1 and 2 (SOSS1 and SOSS2), bind to ssDNA and participate in DNA replication, repair, and recombination processes. Compared to RPA, the SOSS1 complex has a lower affinity for ssDNA binding .…”
Section: Introductionmentioning
confidence: 99%
“…DNA double-strand breaks (DSBs) are one of the most cytotoxic lesions caused by endogenous damaging events such as replication stress, reactive oxygen species, and exogenous agents such as ionizing radiation (IR) and chemical agents. 1 3 If not repaired or improperly repaired, the damaged DNA can cause abnormalities in cellular functions and disease progression. 4 , 5 The DSBs occurring in the G2 phase of the cell cycle are mainly repaired by the error-free, homologous recombination (HR)-mediated repair pathway.…”
Section: Introductionmentioning
confidence: 99%
“…Genome instability with increased DNA double strand breaks (DSBs) is detrimental to neurons of the brain and has been implicated in diverse neurodegenerative disorders (NDs) [1][2][3][4][5][6] . However, the etiology of NDs is multifaceted, the progressive decline in number and activity of neurons exhibits significant comorbidity with glial and cerebrovascular abnormalities [7][8][9][10] .…”
Section: Introductionmentioning
confidence: 99%