Contributions of DNA Damage to Alzheimer’s Disease
Open accessAbstract
Alzheimer’s disease (AD) is the most common type of neurodegenerative disease. Its typical pathology consists of extracellular amyloid-β (Aβ) plaques and intracellular tau neurofibrillary tangles. Mutations in the APP, PSEN1, and PSEN2 genes increase Aβ production and aggregation, and thus cause early onset or familial AD. Even with this strong genetic evidence, recent studies support AD to result from complex etiological alterations. Among them, aging is the strongest risk factor for the vast majority of AD cases: Sporadic late onset AD (LOAD). Accumulation of DNA damage is a well-established aging factor. In this regard, a large amount of evidence reveals DNA damage as a critical pathological cause of AD. Clinically, DNA damage is accumulated in brains of AD patients. Genetically, defects in DNA damage repair resulted from mutations in the BRAC1 and other DNA damage repair genes occur in AD brain and facilitate the pathogenesis. Abnormalities in DNA damage repair can be used as diagnostic biomarkers for AD. In this review, we discuss the association, the causative potential, and the biomarker values of DNA damage in AD pathogenesis.
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DNA repair, Myc targets V1, and oxidative phosphorylation gene sets are linked to cellular damage or stress facilitating the progression of pathogenesis and contributing to neurodegeneration in AD.
“Conversely, 5xFAD-Dp16 also exhibited greatly decreased NES for several gene sets, including DNA repair, Myc targets V1, and oxidative phosphorylation, all of which are linked to cellular damage or stress facilitating the progression of the pathogenesis and contributing to neurodegeneration in AD48,49,50 (Figures 3A and S3A).”
From Interferon signaling modulates Down syndrome-associated Alzheimer’s disease pathology in a mouse model (2025) · cites this paper as [49]
The Conclusions (page not available in our copy) link DNA damage and abnormalities in DNA repair to AD pathogenesis and neurodegeneration. The paper does not establish the claimed links for the Myc targets V1 or oxidative phosphorylation gene sets; searches for those terms found no supporting discussion. (LLM, conf=0.86)
Experimental — accuracy not yet measured5xFAD-Dp16 exhibited greatly decreased NES for several gene sets, including DNA repair, Myc targets V1, and oxidative phosphorylation.
“Conversely, 5xFAD-Dp16 also exhibited greatly decreased NES for several gene sets, including DNA repair, Myc targets V1, and oxidative phosphorylation, all of which are linked to cellular damage or stress facilitating the progression of the pathogenesis and contributing to neurodegeneration in AD48,49,50 (Figures 3A and S3A).”
From Interferon signaling modulates Down syndrome-associated Alzheimer’s disease pathology in a mouse model (2025) · cites this paper as [49]
Section 2 (page unavailable) links impaired DNA repair and accumulated DNA damage to AD pathogenesis, supporting the sentence’s background point about cellular damage. The paper does not report decreased NES in 5xFAD-Dp16 for DNA repair, Myc targets V1, or oxidative phosphorylation; those specific results are not supported by this source. (LLM, conf=0.84)
Experimental — accuracy not yet measuredOxidative DNA damage and mitochondrial dysfunction are thought to contribute to neurodegeneration of AD, vascular dementia, HD, PD and epilepsy.
“Oxidative DNA damage and mitochondrial dysfunction are thought to contribute to the neurodegeneration of AD [75,76], vascular dementia [77], HD [78], PD [79] and epilepsy [80].”
From Rlip76: An Unexplored Player in Neurodegeneration and Alzheimer’s Disease? (2022) · cites this paper as [75]
The cited source is attached to the AD portion of the sentence, not to the separately cited claims about vascular dementia, HD, PD, or epilepsy. Section 2, “Association of DNA Damage with Alzheimer’s Disease” (page unavailable), supports a contribution of oxidative DNA damage to AD pathogenesis. The retrieved passages do not establish the additional claim that mitochondrial dysfunction contributes to AD neurodegeneration; a reference title mentioning it is not enough. (LLM, conf=0.84)
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Cyclin-Dependent Kinases in Brain Development and Disease
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“Increase of 8‐OHdG in ventricular cerebrospinal fluid (CSF) was observed in AD brains, suggesting a biomarker value of 8‐OHdG in AD diagnosis [58].”
BackgroundDown syndrome and Alzheimer's disease: common pathways, common goals
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Increased oxidative damage in nuclear and mitochondrial DNA in mild cognitive impairment
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Increased poly(ADP-ribosyl)ation of nuclear proteins in Alzheimer's disease
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“BRCA1 plays an essential role in HR-mediated repair of DSB [80,84,85,200].”
BackgroundRapid accumulation of genome rearrangements in liver but not in brain of old mice
Dollé, M. E. T., Giese, H., Hopkins, C. L., Martus, H., Hausdorff, J. M., & Vijg, J. (1997) · Nature Genetics · doi:10.1038/ng1297-431 · Cited by 248 · cited 2× · see citing works
“The mutation rate increases following aging in mouse liver but not in the animal brain [40], thus mouse models of AD likely have major limitations in studying aging process of LOAD.”
BackgroundNeuronal cell cycle: the neuron itself and its circumstances
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Early neuronal accumulation of DNA double strand breaks in Alzheimer’s disease
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“Reduction in DSB repair will lead to DSB accumulation, neuron loss, cognitive decline, and thus AD [44,78,79].”
BackgroundThe viral protein corona directs viral pathogenesis and amyloid aggregation
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“HSV-1 induces AD via affecting multiple AD events, such as through enhancing Aβ1−42 production [104].”
BackgroundDNA damage in neurodegenerative diseases
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“Nonetheless, it is becoming increasingly clear that complex pathological etiology instead of the amyloid-cascade hypothesis is involved in LOAD, which accounts for more than 90% of AD cases in patients over 65 year old [32,33].”
BackgroundTranscriptional elongation requires DNA break-induced signalling
Bunch, H., Lawney, B. P., Lin, Y., Asaithamby, A., Murshid, A., Wang, Y. E., Chen, B. P. C., & Calderwood, S. K. (2015) · Nature Communications · doi:10.1038/ncomms10191 · Cited by 203 · see citing works
DNA repair factor BRCA1 depletion occurs in Alzheimer brains and impairs cognitive function in mice
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“Using two independent cohorts (n = 13 and n = 23), significant increases in γH2AX were recently demonstrated in astrocytes and neurons in the hippocampus and frontal cortex of AD brains [44]; the increase occurred in brains with mild cognitive impairment (MCI) [44], a preclinical stage of AD [45,46], suggesting an imp…”
BackgroundA Cdk5 inhibitory peptide reduces tau hyperphosphorylation and apoptosis in neurons
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Harnessing DNA Double-Strand Break Repair for Cancer Treatment
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“BRCA1 plays an essential role in DSB repair using the HR process and recruitment of BRCA1 to DSBs commits cells to HR (Figure 2) [80,86].”
BackgroundResultInfluentialPhosphorylation of ATM by Cdk5 mediates DNA damage signalling and regulates neuronal death
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Silencing of CDK5 Reduces Neurofibrillary Tangles in Transgenic Alzheimer's Mice
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Health Conditions Associated with Aging and End of Life of Adults with Down Syndrome
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“Additionally, DSBs may occur prior to the onset of AD [78,79].”
BackgroundDecreased base excision repair and increased helicase activity in Alzheimer's disease brain
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Evidence of DNA damage in Alzheimer disease: phosphorylation of histone H2AX in astrocytes
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“Elevations in γH2AX, a well-established marker of DSB [42], were detected in 11 of 13 AD brains in astrocytes of hippocampus and cerebral cortex [43].”
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DNA strand breaks in Alzheimer’s disease
Adamec, E., Vonsattel, J. P., & Nixon, R. A. (1999) · Brain Research · doi:10.1016/s0006-8993(99)02004-1 · Cited by 167 · cited 2× · see citing works
“Furthermore, DSBs and single strand breaks (SSBs) were demonstrated at the DNA level in hippocampi of AD brains [47].”
BackgroundNeuroprotective Functions for the Histone Deacetylase SIRT6
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Genome integrity and disease prevention in the nervous systemPreprint
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“Brain is particularly vulnerable to impairment in DNA repair [62], which is likely attributable to the high levels of metabolism and transcription activities in neurons of the central nervous system (CNS) [48,49,63].”
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Essential roles for the FE65 amyloid precursor protein‐interacting proteins in brain development
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Chromosome Missegregation and Trisomy 21 Mosaicism in Alzheimer's Disease
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Herpes Simplex Virus Type 1 in Alzheimer's Disease: The Enemy Within
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“In line with HSV‐1 infection as a well‐recognized risk factor of AD [102,103] in part via inducing DSB accumulation in neurons [105], the virus stimulates CDK5 activation, changes its subcellular location, and induces γH2AX nuclear foci (DSB marker) in infected mouse neurons [167].”
BackgroundA hippocampal Cdk5 pathway regulates extinction of contextual fear
Sananbenesi, F., Fischer, A., Wang, X., Schrick, C., Neve, R. L., Radulović, J., & Tsai, L. (2007) · Nature Neuroscience · doi:10.1038/nn1943 · Cited by 141 · see citing works
Oxidative genome damage and its repair: implications in aging and neurodegenerative diseases
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X chromosome aneuploidy in the Alzheimer’s disease brain
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Transcription-Coupled DNA Double-Strand Break Repair: Active Genes Need Special Care
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“In addition to ROS as a source of DSBs in neurons of CSN, recent development reveals an essential association of transcription with DSB [64].”
BackgroundDNA polymerase β deficiency leads to neurodegeneration and exacerbates Alzheimer disease phenotypes
Sýkora, P., Misiak, M., Wang, Y., Ghosh, S., Leandro, G. D. S., Liu, D., Tian, J. Y., Baptiste, B. A., Cong, W., Brenerman, B. M., et al. (2014) · Nucleic Acids Research · doi:10.1093/nar/gku1356 · Cited by 136 · see citing works
The role of DNA repair in brain related disease pathology
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“Collectively, evidence favors a critical role of BRCA1 in DSB repair in CNS neurons and its dysfunction contributes to DSB accumulation and AD pathogenesis.”
BackgroundInfluentialThe neurological phenotype of ataxia-telangiectasia: Solving a persistent puzzle
Biton, S., Barzilai, A., & Shiloh, Y. (2008) · DNA repair · doi:10.1016/j.dnarep.2008.03.006 · Cited by 133 · cited 2× · see citing works
“Ataxia telangiectasia (AT) is caused by mutations in the ATM gene; the disease manifests defects in multiple system including its typical clinical presentation of ataxia due to progressive neurodegeneration that occurs in early childhood [87].”
BackgroundThe Role of Epigenetic Mechanisms in the Regulation of Gene Expression in the Nervous System
Cholewa-Waclaw, J., Bird, A. P., von Schimmelmann, M. J., Schaefer, A., Yu, H., Song, H., Madabhushi, R., & Tsai, L. (2016) · Journal of Neuroscience · doi:10.1523/jneurosci.2492-16.2016 · Cited by 132 · cited 1× · see citing works
“DSBs occur in the promoters of several early response genes and contribute to their transcription [65]; early response genes function in learning and memory [67,68] suggesting an association of DSB accumulation with cognitive decline, a major defect in patients with AD.”
BackgroundSnider, B. J., Norton, J. B., Coats, M. A., Chakraverty, S., Hou, C. E., Jervis, R., Lendon, C. L., Goate, A., McKeel, D. W., & Morris, J. C. (2005) · Archives of Neurology · doi:10.1001/archneur.62.12.1821 · Cited by 129 · cited 1× · see citing works
“Individuals with these mutations develop early onset dementia in an autosomal-dominant manner [20]; the typical onset starts between 30 and 50 years of age in PSEN1 mutant carriers with some being affected at in their 20s [20,21].”
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Identification and characterization of OGG1 mutations in patients with Alzheimer's disease
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Oxidatively modified nucleic acids in preclinical Alzheimer's disease (PCAD) brain
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“In this regard, accumulation of DNA oxidization was observed in AD brains [51,52]; the lesion was also detected in brains with MCI [53–55] and preclinical AD (PCAD) [55,56].”
BackgroundInfluentialTeixeira, J. P., de Castro, A. A., Soares, F. V., da Cunha, E. F. F., & Ramalho, T. C. (2019) · Molecules · doi:10.3390/molecules24234410 · Cited by 122 · cited 2× · see citing works
“The 40 residue Aβ peptide (Aβ1-40) is the major product, accounting for more than 50% of Aβ peptides [9,17].”
BackgroundGenome instability in Alzheimer disease
Hou, Y., Song, H., Croteau, D. L., Akbari, M., & Bohr, V. A. (2017) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2016.04.005 · Cited by 120 · cited 1× · see citing works
“The topic of “DNA and neurodegenerative diseases” has been previously reviewed [14,30,37].”
BackgroundPetr, M. A., Tulika, T., Carmona-Marin, L. M., & Scheibye‐Knudsen, M. (2020) · Trends in Cell Biology · doi:10.1016/j.tcb.2019.12.001 · Cited by 119 · cited 1× · see citing works
“Aging is clearly a complex process; nonetheless, accumulative evidence reveals a central role of DNA damage in aging [36].”
BackgroundNeurons in Vulnerable Regions of the Alzheimer’s Disease Brain Display Reduced ATM Signaling
Shen, X., Chen, J., Li, J., Kofler, J., & Herrup, K. (2016) · eNeuro · doi:10.1523/eneuro.0124-15.2016 · Cited by 118 · cited 4× · see citing works
“In comparison to age‐matched control subjects, reductions in both the ATM protein and its mRNA were detected in the front cortex of AD brains (n = 9, 5 males and 4 females) [88].”
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The role of Cdk5-mediated apurinic/apyrimidinic endonuclease 1 phosphorylation in neuronal death
Huang, E., Qu, D., Zhang, Y., Venderová, K., Haque, M. E., Rousseaux, M. W. C., Slack, R. S., Woulfe, J., & Park, D. S. (2010) · Nature Cell Biology · doi:10.1038/ncb2058 · Cited by 114 · see citing works
Tissue-specific alternative splicing in the human INK4a/ARF cell cycle regulatory locus
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Nucleic acid oxidation: an early feature of Alzheimer's disease
Bradley‐Whitman, M. A., Timmons, M. D., Beckett, T. L., Murphy, M. P., Lynn, B. C., & Lovell, M. A. (2014) · Journal of Neurochemistry · doi:10.1111/jnc.12444 · Cited by 112 · cited 8× · see citing works
“In this regard, accumulation of DNA oxidization was observed in AD brains [51,52]; the lesion was also detected in brains with MCI [53–55] and preclinical AD (PCAD) [55,56].”
BackgroundInfluentialEstrogen receptor α-mediated transcription induces cell cycle-dependent DNA double-strand breaks
Williamson, L. M., & Lees‐Miller, S. P. (2010) · Carcinogenesis · doi:10.1093/carcin/bgq255 · Cited by 111 · see citing works
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Poly(ADP-ribose) Polymerase-1 in Amyloid Beta Toxicity and Alzheimer's Disease
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DNA damage in the oligodendrocyte lineage and its role in brain aging
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Is DNA repair compromised in Alzheimer’s disease?
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“In sporadic LOAD cases, aging is the strongest risk factor [30,35].”
BackgroundBmi1 regulates murine intestinal stem cell proliferation and self-renewal downstream of Notch
López‐Arribillaga, E., Rodilla, V., Pellegrinet, L., Guiu, J., Iglesias, M., Román, Á., Gutarra, S., González, S., Muñoz‐Cánoves, P., Fernández‐Salguero, P. M., et al. (2014) · Development · doi:10.1242/dev.107714 · Cited by 102 · see citing works
Repair of 8-oxoG:A mismatches by the MUTYH glycosylase: Mechanism, metals and medicine
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“Additionally, TOP2β is expressed in differentiation cells and neurons [74,75]; the expression of long-transcripts linked to autism is facilitated by TOP2β [76].”
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RAD52 is required for RNA-templated recombination repair in post-mitotic neurons
Welty, S., Teng, Y., Liang, Z., Zhao, W., Sanders, L. H., Greenamyre, J. T., Rubio, M. E., Thathiah, A., Kodali, R. B., Wetzel, R. B., et al. (2017) · Journal of Biological Chemistry · doi:10.1074/jbc.m117.808402 · Cited by 98 · cited 1× · see citing works
“This possibility is further supported b induction of the HR protein RAD52 by nascent mRNAs in terminally differentiated neurons and Aβ inhibits RAD52 expression [90].”
BackgroundOligodendroglial Cells in Alzheimer’s Disease
Butt, A. M., Rocha, I. C. D. L., & Rivera, A. D. (2019) · Advances in experimental medicine and biology · doi:10.1007/978-981-13-9913-8_12 · Cited by 95 · see citing works
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Śliwińska, A., Kwiatkowski, D., Czarny, P. L., Toma, M. M., Wigner, P., Drzewoski, J., Fabianowska‐Majewska, K., Szemraj, J., Maes, M. H. J., Gałecki, P., et al. (2016) · Journal of the Neurological Sciences · doi:10.1016/j.jns.2016.07.008 · Cited by 92 · see citing works
p53-dependent SIRT6 expression protects Aβ42-induced DNA damage
Jung, E. S., Choi, H., Song, H., Hwang, Y. J., Kim, A., Ryu, H., & Mook‐Jung, I. (2016) · Scientific Reports · doi:10.1038/srep25628 · Cited by 89 · see citing works
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“In line with HSV‐1 infection as a well‐recognized risk factor of AD [102,103] in part via inducing DSB accumulation in neurons [105], the virus stimulates CDK5 activation, changes its subcellular location, and induces γH2AX nuclear foci (DSB marker) in infected mouse neurons [167].”
BackgroundRapid phosphorylation of histone H2A.X following ionotropic glutamate receptor activation
Crowe, S. L., Movsesyan, V. A., Jorgensen, T. J., & Kondratyev, A. D. (2006) · European Journal of Neuroscience · doi:10.1111/j.1460-9568.2006.04768.x · Cited by 87 · cited 2× · see citing works
“As high transcription activity in post-mitotic neurons remains a major source of DSBs associated with neuron activities and transcription [63,65,66], it seems logical for defects in NHEJ being favored over HR leading to DSB accumulation in AD.”
BackgroundDNA double strand break repair, aging and the chromatin connection
Gorbunova, V., & Seluanov, A. (2016) · Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis · doi:10.1016/j.mrfmmm.2016.02.004 · Cited by 87 · cited 1× · see citing works
“While it is indeed intriguing for an essential role of DSBs at least in a subset of gene transcription, it is clear that DSBs need to be effectively repaired regardless of their sources of generation owning to their toxic impact on genome stability [77].”
BackgroundBrasnjevic, I., Hof, P. R., Steinbusch, H. W. M., & Schmitz, C. (2008) · DNA repair · doi:10.1016/j.dnarep.2008.03.010 · Cited by 86 · cited 1× · see citing works
“By using autoradiographic methods to examine DNA damage (SSB) and repair capacity in neurons, an inverse association of accumulation of nuclear DNA (nDNA) breaks and nDNA repair was documented in aging mouse brain [59,60]; accumulation of nDNA SSB was detected in mouse cerebellar granule cells as well as hippocampal p…”
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Telomeres: Implications for Cancer Development
Bernal, A., & Tusell, L. (2018) · International Journal of Molecular Sciences · doi:10.3390/ijms19010294 · Cited by 86 · see citing works
Histopathology and APOE genotype of the first Alzheimer disease patient, Auguste D.
Graeber, M. B., Kösel, S., Grasbon-Frodl, E. M., Möller, H. ‐., & Mehraein, P. (1998) · Neurogenetics · doi:10.1007/s100480050033 · Cited by 82 · cited 1× · see citing works
“AD was first described by Alois Alzheimer more than one century ago on a patient named Auguste D [1]; the typical pathological features include extensive cerebral amyloid plaques and neurofibrillary tangles [2,3].”
BackgroundCanugovi, C., Yoon, J. S., Feldman, N. H., Croteau, D. L., Mattson, M. P., & Bohr, V. A. (2012) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1204156109 · Cited by 81 · see citing works
The aging brain: Accumulation of DNA damage or neuron loss?
Rutten, B. P. F., Schmitz, C., Gerlach, O. H. H., Oyen, H. M., de Mesquita, E. B., Steinbusch, H. W. M., & Korr, H. (2005) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2005.10.019 · Cited by 80 · cited 1× · see citing works
“By using autoradiographic methods to examine DNA damage (SSB) and repair capacity in neurons, an inverse association of accumulation of nuclear DNA (nDNA) breaks and nDNA repair was documented in aging mouse brain [59,60]; accumulation of nDNA SSB was detected in mouse cerebellar granule cells as well as hippocampal p…”
MethodTrotter, K. W., King, H. A., & Archer, T. (2015) · Molecular and Cellular Biology · doi:10.1128/mcb.00230-15 · Cited by 79 · cited 1× · see citing works
“Subsequently, glucocorticoid receptor was also reported to transactivate genes via TOP2β-produced DSBs [73].”
BackgroundmiR-34a in Neurophysiology and Neuropathology
Chua, C. E. L., & Tang, B. L. (2018) · Journal of Molecular Neuroscience · doi:10.1007/s12031-018-1231-y · Cited by 79 · see citing works
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Mutational spectrum at GATA1 provides insights into mutagenesis and leukemogenesis in Down syndrome
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An anticlastogenic function for the Polycomb Group gene Bmi1
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Cdk5 at crossroads of protein oligomerization in neurodegenerative diseases: facts and hypotheses
Wilkaniec, A., Czapski, G. A., & Adamczyk, A. (2015) · Journal of Neurochemistry · doi:10.1111/jnc.13365 · Cited by 68 · see citing works
A Novel Aspect of Tumorigenesis—BMI1 Functions in Regulating DNA Damage Response
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Self-citationModeling Late-Onset Sporadic Alzheimer’s Disease through BMI1 Deficiency
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Hyperphosphorylation Results in Tau Dysfunction in DNA Folding and Protection
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Cdk5 links with DNA damage response and cancer
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“Furthermore, CDK5 activities affect DNA damage response [12], supporting a linkage of DNA damage with AD [13,14].”
BackgroundMartire, S., Fuso, A., Mosca, L., Forte, E., Correani, V., Fontana, M., Scarpa, S., Maras, B., & D’Erme, M. (2016) · Journal of Alzheimer s Disease · doi:10.3233/jad-151040 · Cited by 62 · see citing works
Base excision DNA repair levels in mitochondrial lysates of Alzheimer's disease
Canugovi, C., Shamanna, R. A., Croteau, D. L., & Bohr, V. A. (2014) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2014.01.004 · Cited by 61 · see citing works
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Reanalysis of the first case of Alzheimer’s disease
Graeber, M. B., & Mehraein, P. (1999) · European Archives of Psychiatry and Clinical Neuroscience · doi:10.1007/pl00014167 · Cited by 59 · see citing works
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Expression of the Fe65 adapter protein in adult and developing mouse brain
Kesavapany, S., Banner, S. J., Lau, K., Shaw, C. E., Miller, C. C. J., Cooper, J. D., & McLoughlin, D. M. (2002) · Neuroscience · doi:10.1016/s0306-4522(02)00422-0 · Cited by 57 · cited 1× · see citing works
“FE65 is an adaptor protein with its expression enriched in the brain [94,95].”
BackgroundTse, K., Cheng, A., Ma, F., & Herrup, K. (2018) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2017.11.010 · Cited by 56 · see citing works
Mechanisms and consequences of aneuploidy and chromosome instability in the aging brain
Andriani, G. A., Vijg, J., & Montagna, C. (2016) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2016.03.007 · Cited by 55 · see citing works
Evaluation of the poly(ADP‐ribose) polymerase‐1 gene variants in Alzheimer's disease
Liu, H., Lin, W., Wu, B., Liu, S. R., Wang, W., Tsai, C., Lee, C., & Tsai, F. (2010) · Journal of Clinical Laboratory Analysis · doi:10.1002/jcla.20379 · Cited by 54 · see citing works
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Sublethal Doses of β-Amyloid Peptide Abrogate DNA-dependent Protein Kinase Activity
Cardinale, A., Racaniello, M., Saladini, S., Chiara, G. D., Mollinari, C., de Stefano, M. C., Pocchiari, M., Garaci, E., & Merlo, D. (2011) · Journal of Biological Chemistry · doi:10.1074/jbc.m111.276550 · Cited by 54 · see citing works
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“Additionally, DSBs may occur prior to the onset of AD [78,79].”
BackgroundZeng, J., Libien, J. M., Shaik, F., Wolk, J., & Hernandez, A. I. (2016) · Neural Plasticity · doi:10.1155/2016/8987928 · Cited by 53 · see citing works
Harkin, L. F., Gerrelli, D., Diaz, D. G., Santos, C., Alzu’bi, A., Austin, C. A., & Clowry, G. J. (2015) · Journal of Anatomy · doi:10.1111/joa.12416 · Cited by 52 · cited 1× · see citing works
“Additionally, TOP2β is expressed in differentiation cells and neurons [74,75]; the expression of long-transcripts linked to autism is facilitated by TOP2β [76].”
BackgroundWężyk, M., Szybińska, A., Wojsiat, J., Szczerba, M., Day, K., Rönnholm, H., Kele, M., Berdyński, M., Pepłońska, B., Fichna, J. P., et al. (2018) · Journal of Alzheimer s Disease · doi:10.3233/jad-170830 · Cited by 51 · cited 9× · see citing works
“In neurons differentiated from induced pluripotent stem cells (iPSC) that were reprogrammed from fibroblasts of familial AD patients, location of BRCA1 to cytosol is also demonstrated [89].”
BackgroundInfluentialMisiak, M., Greeno, R. V., Baptiste, B. A., Sýkora, P., Liu, D., Cordonnier, S. A., Fang, E. F., Croteau, D. L., Mattson, M. P., & Bohr, V. A. (2016) · Aging Cell · doi:10.1111/acel.12541 · Cited by 50 · see citing works
Altered DNA repair; an early pathogenic pathway in Alzheimer’s disease and obesity
Yu, H., Harrison, F. E., & Xia, F. (2018) · Scientific Reports · doi:10.1038/s41598-018-23644-4 · Cited by 50 · cited 3× · see citing works
“In the APP/PSEN1 mouse model for AD, a decrease in the HR protein RAD51 co-exists with DSB accumulation [91].”
BackgroundInfluentialModeling an Anti-Amyloid Combination Therapy for Alzheimer's Disease
Chow, V. W., Savonenko, A., Melnikova, T., Kim, H., Price, D., Li, T., & Wong, P. (2010) · Science Translational Medicine · doi:10.1126/scitranslmed.3000337 · Cited by 48 · see citing works
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Neuron loss during early adulthood following prenatal low-dose X-irradiation in the mouse brain
Korr, H. (2001) · International Journal of Radiation Biology · doi:10.1080/09553000010028467 · Cited by 47 · cited 1× · see citing works
“By using autoradiographic methods to examine DNA damage (SSB) and repair capacity in neurons, an inverse association of accumulation of nuclear DNA (nDNA) breaks and nDNA repair was documented in aging mouse brain [59,60]; accumulation of nDNA SSB was detected in mouse cerebellar granule cells as well as hippocampal p…”
MethodNAD attenuates oxidative DNA damages induced by amyloid beta-peptide in primary rat cortical neurons
Wu, M.-H., Yin, J., Hwang, C.-S., Tang, C.-M., & Yang, D. (2014) · Free Radical Research · doi:10.3109/10715762.2014.907889 · Cited by 46 · see citing works
Altered DNA base excision repair profile in brain tissue and blood in Alzheimer’s disease
Lillenes, M. S., Rabano, A., Støen, M., Riaz, T., Misaghian, D., Møllersen, L., Esbensen, Y., Günther, C.-C., Selnes, P., Stenset, V. T. V., et al. (2016) · Molecular Brain · doi:10.1186/s13041-016-0237-z · Cited by 46 · see citing works
Chromosome Instability in the Neurodegenerating Brain
Yurov, Y. B., Vorsanova, S. G., & Iourov, I. Y. (2019) · Frontiers in Genetics · doi:10.3389/fgene.2019.00892 · Cited by 45 · see citing works
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Molecular mechanisms of aging and anti-aging strategies
Li, Y., Tian, X., Luo, J., Bao, T., Wang, S., & Wu, X. (2024) · Cell Communication and Signaling · doi:10.1186/s12964-024-01663-1 · Cited by 333 · see citing works
“…breakdown of repair functions, eventually leading to the loss of cell and organ function and promoting the occurrence and development of age-related diseases disease [53], Alzheimer’s disease [54], and cancer [55], suggesting that DNA damage is directly related to the incidence of these diseases.”
BackgroundNeurogenesis in aging and age-related neurodegenerative diseases
Čulig, L., Chu, X., & Bohr, V. A. (2022) · Ageing Research Reviews · doi:10.1016/j.arr.2022.101636 · Cited by 229 · see citing works
Alzheimer’s Disease: Exploring the Landscape of Cognitive Decline
Tenchov, R., Sasso, J. M., & Zhou, Q. A. (2024) · ACS Chemical Neuroscience · doi:10.1021/acschemneuro.4c00339 · Cited by 170 · see citing works
The role of PARP1 in neurodegenerative diseases and aging
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Redox dysregulation as a driver for DNA damage and its relationship to neurodegenerative diseases
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“Several mechanisms have been implicated in the pathogenesis, including both oxidative stress and DNA damage [236, 240].”
BackgroundTeixeira, J. P., de Castro, A. A., Soares, F. V., da Cunha, E. F. F., & Ramalho, T. C. (2019) · Molecules · doi:10.3390/molecules24234410 · Cited by 122 · see citing works
Genomics of Alzheimer’s disease implicates the innate and adaptive immune systems
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miR-34a in Neurophysiology and Neuropathology
Chua, C. E. L., & Tang, B. L. (2018) · Journal of Molecular Neuroscience · doi:10.1007/s12031-018-1231-y · Cited by 79 · see citing works
Importance of Bioactive Substances in Sheep’s Milk in Human Health
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“Accumulation of DNA damage is a well-known factor of aging and, therefore, is believed to be the main cause of Alzheimer’s disease [77].”
BackgroundMyelin in Alzheimer’s disease: culprit or bystander?
Maitre, M., Jeltsch-David, H., Okechukwu, N. G., Klein, C., Patte-Mensah, C., & Mensah-Nyagan, A.-G. (2023) · Acta Neuropathologica Communications · doi:10.1186/s40478-023-01554-5 · Cited by 66 · see citing works
Transposable elements as new players in neurodegenerative diseases
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The Complex Mechanisms by Which Neurons Die Following DNA Damage in Neurodegenerative Diseases
Shadfar, S., Brocardo, M. G., & Atkin, J. D. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23052484 · Cited by 54 · see citing works
“Several mechanisms are implicated in the pathophysiology of Alzheimer’s disease, including Aβ deposition [152], tau hyperphosphorylation [152], neuroinflammation [150], constriction of brain capillaries [153], Aβ interaction with hippocampal ghrelin/GHSR1α signalling [154], DNA damage [155], disrupted RNA hemostasias…”
BackgroundThe Role of DNA Damage in Neural Plasticity in Physiology and Neurodegeneration
Konopka, A., & Atkin, J. D. (2022) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2022.836885 · Cited by 51 · see citing works
Role of primary aging hallmarks in Alzheimer´s disease
Zhao, J., & Huai, J. (2022) · Theranostics · doi:10.7150/thno.79535 · Cited by 53 · see citing works
“may be an important pathological cause of AD, particularly in LOAD cases [21, 31, 32].”
BackgroundChromosome Instability, Aging and Brain Diseases
Iourov, I. Y., Yurov, Y. B., Vorsanova, S. G., & Kutsev, S. I. (2021) · Cells · doi:10.3390/cells10051256 · Cited by 51 · see citing works
“Uncor‐ rected DNA damage, which is able to initiate CIN, is also a biomarker of Alzheimer’s disease [48].”
BackgroundDNA Double-Strand Breaks as Pathogenic Lesions in Neurological Disorders
Provasek, V. E., Mitra, J., Malojirao, V. H., & Hegde, M. L. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23094653 · Cited by 51 · see citing works
“Alternatively, these tissues demonstrate decreased expression of RAD51, an HR-associated repair factor [202,203].”
BackgroundZhang, X., Yuan, T., Chen, X., Liu, X., Hu, J., & Liu, Z. (2023) · Progress in Lipid Research · doi:10.1016/j.plipres.2023.101256 · Cited by 50 · see citing works
Malfatti, M. C., Antoniali, G., Codrich, M., & Tell, G. (2021) · DNA repair · doi:10.1016/j.dnarep.2021.103133 · Cited by 44 · see citing works
Poly (ADP-ribose) polymerase 1 and neurodegenerative diseases: past, present, and future
Hu, M.-L., Pan, Y.-R., Yong, Y.-Y., Liu, Y., Yu, L., Qin, D.-L., Qiao, G., Law, B. Y.-K., Wu, J.-M., Zhou, X.-G., et al. (2023) · Ageing Research Reviews · doi:10.1016/j.arr.2023.102078 · Cited by 44 · see citing works
Pereira, T. D. M. C., Côco, L. Z., Ton, A. M. M., Meyrelles, S. S., Campos‐Toimil, M., Campagnaro, B. P., & Vasquez, E. C. (2021) · Antioxidants · doi:10.3390/antiox10111845 · Cited by 42 · see citing works
DNA Damage-Mediated Neurotoxicity in Parkinson’s Disease
Wang, Z., Li, Y., Pu, J., & Zhang, B. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24076313 · Cited by 39 · see citing works
Pro-Aging Effects of Xanthine Oxidoreductase Products
Battelli, M. G., Bortolotti, M., Bolognesi, A., & Polito, L. (2020) · Antioxidants · doi:10.3390/antiox9090839 · Cited by 38 · see citing works
“High levels of ROS induce oxidative stress, leading to advanced glycation endproducts (AGE) accumulation [20], insoluble protein aggregation [21], lipid peroxidation [22] and nucleic acid damage [23].”
BackgroundR-loop Mediated DNA Damage and Impaired DNA Repair in Spinal Muscular Atrophy
Cuartas, J., & Gangwani, L. (2022) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2022.826608 · Cited by 38 · see citing works
“TC-NER-mediated R-loop processing used to minimize transcriptional stress can create further DNA damage and R-loop accumulation (Lin and Wilson, 2012; Lans et al., 2019; Nakazawa et al., 2020).”
BackgroundcGAS-STING signalling regulates microglial chemotaxis in genome instability
Talbot, E., Joshi, L., Thornton, P., Dezfouli, M., Tsafou, K., Perkinton, M. S., & Khoronenkova, S. V. (2023) · Nucleic Acids Research · doi:10.1093/nar/gkad1184 · Cited by 35 · see citing works
Cellular Senescence in Traumatic Brain Injury: Evidence and Perspectives
Schwab, N., Leung, E., & Hazrati, L. (2021) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2021.742632 · Cited by 33 · see citing works
Bartholomew, S. K., Winslow, W., Sharma, R., Pathak, K. V., Tallino, S., Judd, J. M., Leon, H., Turk, J., Pirrotte, P., & Velazquez, R. (2024) · Journal of Neuroinflammation · doi:10.1186/s12974-024-03290-6 · Cited by 28 · see citing works
“Impaired repair of oxidative DNA damage has been linked to the development and progression of AD [107, 108].”
Nuclear dynamics and stress responses in Alzheimer’s disease
Iatrou, A., Clark, E. M., & Wang, Y. (2021) · Molecular Neurodegeneration · doi:10.1186/s13024-021-00489-6 · Cited by 27 · see citing works
“If the damage remains unrepaired, genome instability, cellular senescence, and cell death can subsequently occur [84, 85] .”
BackgroundCardillo, M., Katam, K., & Suravajhala, P. (2025) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2025.1591796 · Cited by 27 · see citing works
“Additionally, age-related DNA damage that occurs during the expression of learning-related genes may accelerate the progression of AD (Lin et al., 2020).”
The Potential Roles of Redox Enzymes in Alzheimer’s Disease: Focus on Thioredoxin
Jia, J., Zeng, X., Xu, G., & Wang, Z. (2021) · ASN NEURO · doi:10.1177/1759091421994351 · Cited by 26 · see citing works
Rahman, M. A., Khatun, M. T., Mim, A. K., Khandocar, M. P., Rahman, A., Hasan, M. H., Shimki, A. I., Hossain, M. S., Shoily, M. S. A., Faraque, A., et al. (2025) · Cell Biochemistry and Biophysics · doi:10.1007/s12013-025-01845-9 · Cited by 26 · see citing works
“Impaired DNA repair mechanisms, including mutations in genes like BRCA 1 , contribute to AD progression and may serve as biomarkers [84].”
SIRT6 Through the Brain Evolution, Development, and Aging
García-Venzor, A., & Toiber, D. (2021) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2021.747989 · Cited by 26 · see citing works
“DNA methylation is one of the main epigenetic mechanisms that repress the expression of genes at specific developmental stages; it is required at both stages in NPCs and neurons (Costello, 2003; Numata et al., 2012; Lister et al., 2013).”
BackgroundA mitotic CDK5-PP4 phospho-signaling cascade primes 53BP1 for DNA repair in G1
Zheng, X.-F., Acharya, S. S., Choe, K. N., Nikhil, K., Adelmant, G., Satapathy, S. R., Sharma, S., Viccaro, K., Rana, S., Natarajan, A., et al. (2019) · Nature Communications · doi:10.1038/s41467-019-12084-x · Cited by 24 · see citing works
Singh, A., Tiwari, S., & Singh, S. (2024) · Cell Death and Disease · doi:10.1038/s41419-024-06662-1 · Cited by 23 · see citing works
“However, there are several other known factors which are known to contribute in these neurodegenerative mechanisms therefore, the con fl ated investigation is still require to consider the Pirh2 as therapeutic target for the AD management.”
BackgroundCauses and Consequences of Genome Instability in Psychiatric and Neurodegenerative Diseases
Iourov, I. Y., Vorsanova, S. G., Куринная, О. С., Zelenova, M. A., Vasin, K. S., & Yurov, Y. B. (2021) · Molecular Biology · doi:10.1134/s0026893321010155 · Cited by 20 · see citing works
Tian, Z., Huang, K., Yang, W., Chen, Y., Lyv, W., Zhu, B., Yang, X., Ma, P., & Tong, Z. (2024) · Cell Biology and Toxicology · doi:10.1007/s10565-024-09926-w · Cited by 19 · see citing works
“…in AD AD is the most common type of dementia, accounting for about 60–70% of the total number of dementia, and has been the subject of much research since its discovery in the twentieth century due to its insidious onset, long course, poor prognosis, and high burden of care (Lin et al. 2020).”
Yashooa, R. K., Nabi, A. Q., Smail, S. W., Azeez, S. S., Nooh, W. A., Mustafa, S. A., Al-Farha, A. A.-B., Capitanio, N., & Shekha, M. S. (2026) · Frontiers in Neurology · doi:10.3389/fneur.2025.1737468 · Cited by 20 · see citing works
Polyzos, A. A., Cheong, A. W. Y., Yoo, J. H., Blagec, L., Toprani, S. M., Nagel, Z. D., & McMurray, C. T. (2024) · Nature Communications · doi:10.1038/s41467-024-51906-5 · Cited by 19 · see citing works
“Furthermore, DSBs are implicated in age-related neurodegenerative diseases, such as Alzheimer ’ s disease (AD) 32 – 34 , Parkinson disease (PD) 35 – 37 , and Amyotrophic lateral sclerosis (ALS) 38 .”
Poly ADP-ribose signaling is dysregulated in Huntington disease
Maiuri, T., Bazan, C. B., Harding, R., Begeja, N., Kam, T., Byrne, L. M., Rodrigues, F. B., Warner, M. M., Neuman, K., Mansoor, M., et al. (2024) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2318098121 · Cited by 19 · see citing works
Premature aging in genetic diseases: what conclusions can be drawn for physiological aging
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“Similarly, to age-dependent dementias and sporadic late onset Alzheimer ’ s disease (LOAD) (Bouhrara et al., 2018; Lin et al., 2020), CS is characterized by neuronal loss with severe demyelination, however with so far no detectable amyloid-beta accumulation and no hyperphosphorylated tau (Woody et…”
BackgroundXie, J., Cheng, J., Ko, H., & Tang, Y. (2024) · EMBO Molecular Medicine · doi:10.1038/s44321-024-00046-w · Cited by 17 · see citing works
“…(OGG1), Breast cancer gene 1(BRCA1), PARP1, and DNA-PKcs, as representatives for basic excision repair (BER), homologous repair (HR), and non-homologous end joining (NHEJ), respectively, are reported to decrease in AD due to aggravating oxidative stress (Lin et al, 2020; Pao et al, 2020).”
BackgroundSomatic mosaicism in the diseased brain
Iourov, I. Y., Vorsanova, S. G., Куринная, О. С., Kutsev, S. I., & Yurov, Y. B. (2022) · Molecular Cytogenetics · doi:10.1186/s13039-022-00624-y · Cited by 17 · see citing works
“DNA damage in neurons may initiate apoptosis or produce a senescence-like state mediated by chromosome instability [113, 114], which may lead to cell death by another mechanism (e.”
BackgroundGlioblastoma and its treatment are associated with extensive accelerated brain aging
Ainslie, A. P., Klaver, M., Voshart, D. C., Gerrits, E., den Dunnen, W. F. A., Eggen, B. J. L., Bergink, S., & Barazzuol, L. (2024) · Aging Cell · doi:10.1111/acel.14066 · Cited by 17 · see citing works
“DNA damage and reduced expression of DNA damage response proteins have also been implicated in AD (Lin et al., 2020; Sykora et al., 2015 ).”
BackgroundRlip76: An Unexplored Player in Neurodegeneration and Alzheimer’s Disease?
Hindle, A., Singh, S. P., Pradeepkiran, J. A., Bose, C., Vijayan, M., Kshirsagar, S., Sawant, N. A., & Reddy, P. H. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23116098 · Cited by 14 · see citing works
“Oxidative DNA damage and mitochondrial dysfunction are thought to contribute to the neurodegeneration of AD [75,76], vascular dementia [77], HD [78], PD [79] and epilepsy [80].”
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Emerging Technologies for Genome-Wide Profiling of DNA Breakage
Rybin, M. J., Ramic, M., Ricciardi, N. R., Kapranov, P., Wahlestedt, C., & Zeier, Z. R. (2021) · Frontiers in Genetics · doi:10.3389/fgene.2020.610386 · Cited by 14 · see citing works
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DNA Damage and Chromatin Rearrangement Work Together to Promote Neurodegeneration
Sharma, H., Koirala, S., Chew, Y. L., & Konopka, A. (2024) · Molecular Neurobiology · doi:10.1007/s12035-024-04331-0 · Cited by 14 · see citing works
“β-Amyloid precursor protein (APP) initiates the formation of extracellular amyloid-β (Aβ) in AD [61].”
BackgroundПричины и последствия геномной нестабильности при психических и нейродегенеративных заболеваниях
Yurov, Y. B., Vorsanova, S. G., Куринная, О. С., Zelenova, M. A., Vasin, K. S., & Yurov, Y. B. (2020) · Molecular Biology · doi:10.31857/s0026898421010158 · Cited by 13 · see citing works
Oxidative Stress in the Pathogenesis of Neurodegenerative Diseases
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“The hyperphosphorylated state of tau protein also interferes with the ability of tau to bind to chromatin and protect the genome from oxidative damage, thus enhancing the oxidative damage of DNA [105].”
Welty, S., Thathiah, A., & Levine, A. S. (2022) · Journal of Alzheimer s Disease · doi:10.3233/jad-220030 · Cited by 13 · see citing works
“Inefficient and unfaithful DNA repair can lead to cell cycle arrest, accumulation of detrimental mutations, innate immune system activation, and cell death (reviewed in [23]).”
Exercise May Affect Metabolism in Cancer-Related Cognitive Impairment
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“The association of DNA damage with aging is well-studied [33].”
BackgroundHalder, D., Das, S., Jeyaprakash, R. S., & Joseph, A. (2022) · Journal of Biomolecular Structure and Dynamics · doi:10.1080/07391102.2022.2158136 · Cited by 11 · see citing works
“Quercetin and hesperetin were discovered to upregulate the activity of Akt in preclinical research, resulting in neuronal survival (Khan et al., 2019; Lin et al., 2020).”
BackgroundA Review of PARP-1 Inhibitors: Assessing Emerging Prospects and Tailoring Therapeutic Strategies
Ramesh, S., Almeida, S. D., Hammigi, S., Radhakrishna, G. K., Sireesha, G., Theivendren, P., Vellingiri, S., Kunjiappan, S., Ammunje, D. N., & Pavadai, P. (2023) · Drug Research · doi:10.1055/a-2181-0813 · Cited by 12 · see citing works
“In AD, PARP-1 and SIRT1 contend with one another for a limited supply of NAD + [99–101].”
BackgroundBohr, V. A., Park, J. H., Sahbaz, B. D., Pekhale, K., Chu, X., Okur, M. N., Grati, M., Isgrig, K. T., Chien, W. W., Chrysostomou, E., et al. (2024) · doi:10.59368/agingbio.20240025 · Cited by 11 · see citing works
“DNA damage accumulation is a risk factor for AD, and much evidence suggests that it may have a causative role in AD progression 36,37 .”
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Taskina, D., Zhu, C., Schwab, N., & Hazrati, L. (2024) · Brain Communications · doi:10.1093/braincomms/fcad314 · Cited by 10 · see citing works
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“Additionally, accumulation of damaged DNA has been directly linked to neuronal death in other syndromes, such as Alzheimer’s disease (57, 58).”
BackgroundCytogenomic landscape of the human brain
Iourov, I. Y., Vorsanova, S. G., & Yurov, Y. B. (2021) · Elsevier eBooks · doi:10.1016/b978-0-12-823579-9.00013-8 · Cited by 10 · see citing works
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“It is worth noting that growing evidence indicates that post-mitotic neurons are capable of becoming senescent and DNA damage that accumulates in aging neurons may be an important driving factor of senescence, contributing to both brain aging and possibly AD pathogenesis [42, 44].”
Lai, Y., Han, L., Chen, M., Lin, X., Wu, L., Zhao, Y., Lin, F., & Lin, C. (2023) · Frontiers in Immunology · doi:10.3389/fimmu.2023.1115202 · Cited by 9 · see citing works
“It was found that DDR deficiency caused by mutations in DDR regulators, including BRAC1 occurs in the brain regions of AD and is implicated in the development of pathology (13).”
BackgroundSelf-citationCan accelerated ageing models inform us on age‐related tauopathies?
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“Unsurprisingly, reduced genomic stability has been a widely reported feature in Alzheimer's disease (reviewed by Lin et al., 2020).”
BackgroundHuang, J., Song, Z., Wei, B., Li, Q., Lin, P., Li, H., & Dong, K. (2023) · BMC Psychiatry · doi:10.1186/s12888-023-04634-x · Cited by 9 · see citing works
“DNA damage is a critical pathological cause of AD [34].”
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“Accumulation of DNA damage can elicit excessive apoptosis or cell death of neurons thereby leading to neurological diseases [21–24].”
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“Moreover, oxidative DNA damage [20,21] in the AD brain, tightly connected with Aβ and TAU pathologies [12], seem to occur prior to disease onset [22,23].”
BackgroundNovel molecular mechanisms in Alzheimer’s disease: The potential role of DEK in disease pathogenesis
Greene, A. N., Solomon, M. B., & Vinnedge, L. M. P. (2022) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2022.1018180 · Cited by 7 · see citing works
“Finally, DNA damage is a well-accepted trigger of cell death and apoptosis in AD (Lin et al., 2020).”
BackgroundFISHing for Chromosome Instability and Aneuploidy in the Alzheimer’s Disease Brain
Yurov, Y. B., Vorsanova, S. G., & Iourov, I. Y. (2022) · Methods in molecular biology · doi:10.1007/978-1-0716-2655-9_10 · Cited by 8 · see citing works
Exome sequence analysis of rare frequency variants in Late-Onset Alzheimer Disease
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“Defects in DNA damage and repair enzymes such as RAD54B may facilitate the disease pathogenesis (Murzik et al. 2008; Lin et al. 2020).”
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“In mature brains, neural cells are also prone to DNA damage caused by metabolites including oxygen free radicals, homocysteine and amyloid β-peptide (Aβ) [4,17,19,21].”
BackgroundCellular Reprogramming and Its Potential Application in Alzheimer’s Disease
Zhou, C., Ni, W., Zhu, T., Dong, S., Sun, P., & Hua, F. (2022) · Frontiers in Neuroscience · doi:10.3389/fnins.2022.884667 · Cited by 8 · see citing works
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“Studies have revealed that DNA damage and enzyme system repair defects are associated with the pathogenesis of pulmonary hypertension, systemic lupus erythematosus, Alzheimer ’ s disease, atherosclerosis, aortic disease, and many other diseases [7, 9 – 12].”
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“DNA damage and impaired DNA repair mechanisms have been implicated in the pathogenesis of AD (Lin et al., 2020; Weissman et al., 2007) leading to genomic instability and neuronal death.”
The Biological Intersection Between Chemotherapy-Related Cognitive Impairment and Alzheimer Disease
Torre, M., Zanella, C. A., & Feany, M. Β. (2025) · American Journal Of Pathology · doi:10.1016/j.ajpath.2024.12.013 · Cited by 7 · see citing works
“57 e 59 Brie fl y, AD patients and AD-relevant model systems show elevated oxidative stress, DNA damage, and evidence of mitochondrial dysfunction in the brain, 57 e 59 and these processes are tightly linked and occur early in AD.”
Cacabelos, R. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26157175 · Cited by 8 · see citing works
Drug repurposing using meta-analysis of gene expression in Alzheimer’s disease
Jang, H. Y., Oh, J. M., & Kim, I. (2022) · Frontiers in Neuroscience · doi:10.3389/fnins.2022.989174 · Cited by 8 · see citing works
“For instance, some anti-neoplastic agents can cause DNA damage, which is a critical pathological cause of Alzheimer’s disease (Lin et al., 2020).”
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“These histone modifications are early events, and key for a successful DNA repair (Aricthota et al., 2022; Dhar et al., 2017; Lin et al., 2020).”
BackgroundMicroglial inflammation in genome instability: A neurodegenerative perspective
Maliar, N. L., Talbot, E., Edwards, A. R., & Khoronenkova, S. V. (2024) · DNA repair · doi:10.1016/j.dnarep.2024.103634 · Cited by 5 · see citing works
The many connections of UFMylation with Alzheimer’s disease: a comprehensive review
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Development of a Novel, Automated High-Throughput Device for Performing the Comet Assay
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“Additionally, we observed downregulated homologous recombination and non-homologous end-joining, which are the DNA double- strand-break repair pathways (Lin et al. 2020) that mainly activate during the cell cycle.”
Naffaa, M. M. (2025) · Lifespan development and mental health. · doi:10.70322/ldmh.2025.10005 · Cited by 3 · see citing works
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“BRCA1 knockdown led to increased neuronal DSBs, elevated cell death, and deficits in learning and memory [32].”
InfluentialMechanism, measurement and significance of oxidative DNA damage - a tribute to Miral Dizdaroglu
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“This widely accepted therapeutic potential of PARP1 inhibitors in neurodegenera-tion causing cognitive impairment [27, 29], is challenged by more recent fi ndings.”
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“Defects in the DDR contribute to AD pathogenesis, leading to increased DNA damage and neurodegeneration (Lin et al. 2020; Nelson and Xu 2023).”
COMET Assay for Detection of DNA Damage During Axolotl Tail Regeneration
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“Many researchers are of the opinion that aging and AD may result from the accumulation of unre-paired DNA damages (Lin et al., 2020; Shanbhag et al., 2019; Welch and Tsai, 2022).”
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“2,3 Moreover, when genetic defects occur in the genes responsible for maintaining the normal function of the genome and involved in the repair of DNA double-strand breaks (DSB) and DNA single-strand breaks (SSB), it can lead to transcriptional stalling in neurons and the activation of cell death…”
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“41 As such, a substantial amount of evidence points to DNA damage as a critical player in the pathogenesis AD.”
- Authors
- Lin, X., Kapoor, A., Gu, Y., Chow, M. J., Peng, J., Zhao, K., & Tang, D.
- Affiliations
- St. Joseph’s Healthcare Hamilton (CA)
- Corresponding author
- Tang, Damu
- Venue
- International Journal of Molecular Sciences
- Publisher
- MDPI AG
- Published
- 2020-02-28
- Volume
- 21
- Issue
- 5
- Pages
- 1666
- ISSN
- 1422-0067 (ISSN-L)
- PMC
- PMC7084447
- OpenAlex
- W3009111493
- Cited by
- 117
- References
- 241
- Citations by year
- 2026: 15 · 2025: 19 · 2024: 22 · 2023: 18 · 2022: 19 · 2021: 16 · 2020: 5 · 2019: 2 · 2018: 1
- FWCI
- 1.85
- Type
- journal article
- Language
- en
- Open access
- gold
- dx.doi.org
- Licence
- Locations
- International Journal of Molecular Sciences (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Cancer Research Society (NA)
- Canadian Cancer Society (319412)
- Canadian Institutes of Health Research (NA)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Keywords
- Alzheimer's disease, DNA damage, DNA repair, aging, amyloid plaques, neurofibrillary tangles, BRCA1, familial Alzheimer's disease, late-onset Alzheimer's disease, diagnostic biomarkers, neurodegeneration
- MeSH terms
- Alzheimer Disease, DNA Damage, DNA Repair, Humans, Models, Biological, Risk Factors, Neurogenesis
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