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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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“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]
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“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]
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“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]
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“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.”
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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].”
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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].”
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Herpes Simplex Virus Type 1 in Alzheimer's Disease: The Enemy Within
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X chromosome aneuploidy in the Alzheimer’s disease brain
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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
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“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].”
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“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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“The 40 residue Aβ peptide (Aβ1-40) is the major product, accounting for more than 50% of Aβ peptides [9,17].”
BackgroundOxidatively 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].”
BackgroundInfluentialNeurons in Vulnerable Regions of the Alzheimer’s Disease Brain Display Reduced ATM Signaling
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BackgroundResultInfluentialThe role of Cdk5-mediated apurinic/apyrimidinic endonuclease 1 phosphorylation in neuronal death
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“Aging is clearly a complex process; nonetheless, accumulative evidence reveals a central role of DNA damage in aging [36].”
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Estrogen receptor α-mediated transcription induces cell cycle-dependent DNA double-strand breaks
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Nucleic acid oxidation: an early feature of Alzheimer's disease
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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].”
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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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“In sporadic LOAD cases, aging is the strongest risk factor [30,35].”
BackgroundIs DNA repair compromised in Alzheimer’s disease?
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Bmi1 regulates murine intestinal stem cell proliferation and self-renewal downstream of Notch
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Repair of 8-oxoG:A mismatches by the MUTYH glycosylase: Mechanism, metals and medicine
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RAD52 is required for RNA-templated recombination repair in post-mitotic neurons
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“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].”
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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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Oligodendroglial Cells in Alzheimer’s Disease
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Telomeres: Implications for Cancer Development
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p53-dependent SIRT6 expression protects Aβ42-induced DNA damage
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“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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“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×
“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
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“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].”
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miR-34a in Neurophysiology and Neuropathology
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Histopathology and APOE genotype of the first Alzheimer disease patient, Auguste D.
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“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].”
BackgroundThe 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 81 · cited 1×
“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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“Subsequently, glucocorticoid receptor was also reported to transactivate genes via TOP2β-produced DSBs [73].”
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An anticlastogenic function for the Polycomb Group gene Bmi1
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A Novel Aspect of Tumorigenesis—BMI1 Functions in Regulating DNA Damage Response
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Self-citationMutational spectrum at GATA1 provides insights into mutagenesis and leukemogenesis in Down syndrome
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Leandro, G. D. S., Evangelista, A. F., Lôbo, R. R., Xavier, D. J., Moriguti, J. C., & Sakamoto‐Hojo, E. T. (2018) · Journal of Alzheimer s Disease · doi:10.3233/jad-170205 · Cited by 67
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].”
BackgroundHyperphosphorylation Results in Tau Dysfunction in DNA Folding and Protection
Lü, Y., He, H.-J., Zhou, J., Jun-Ye, M. I. A. O., Lü, J., He, Y.-G., Pan, R., Yan, W., Liu, Y. M., & He, R. (2013) · Journal of Alzheimer s Disease · doi:10.3233/jad-130602 · Cited by 65
Modeling Late-Onset Sporadic Alzheimer’s Disease through BMI1 Deficiency
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Base excision DNA repair levels in mitochondrial lysates of Alzheimer's disease
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Reanalysis of the first case of Alzheimer’s disease
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Expression of the Fe65 adapter protein in adult and developing mouse brain
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BackgroundMechanisms and consequences of aneuploidy and chromosome instability in the aging brain
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Sublethal Doses of β-Amyloid Peptide Abrogate DNA-dependent Protein Kinase Activity
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“Additionally, DSBs may occur prior to the onset of AD [78,79].”
BackgroundModeling an Anti-Amyloid Combination Therapy for Alzheimer’s Disease
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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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“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].”
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Altered DNA repair; an early pathogenic pathway in Alzheimer’s disease and obesity
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“In the APP/PSEN1 mouse model for AD, a decrease in the HR protein RAD51 co-exists with DSB accumulation [91].”
BackgroundInfluentialAberrant Accumulation of BRCA1 in Alzheimer Disease and Other Tauopathies
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“The association of BRCA1 with phosphorylated tau in AD brain was also observed [93], consistent with tau hyperphosphorylation causing tau aggregation.”
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NAD attenuates oxidative DNA damages induced by amyloid beta-peptide in primary rat cortical neurons
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Neuron loss during early adulthood following prenatal low-dose X-irradiation in the mouse brain
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“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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Cited by
Sorted by citations
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 358
“…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 235
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
The role of PARP1 in neurodegenerative diseases and aging
Mao, K., & Zhang, G. (2022) · The FEBS Journal · doi:10.1111/febs.15716 · Cited by 172
Redox dysregulation as a driver for DNA damage and its relationship to neurodegenerative diseases
Shadfar, S., Parakh, S., Jamali, M. S., & Atkin, J. D. (2023) · Translational Neurodegeneration · doi:10.1186/s40035-023-00350-4 · Cited by 148
“Several mechanisms have been implicated in the pathogenesis, including both oxidative stress and DNA damage [236, 240].”
Background
Metadata
- 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
- 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
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › 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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