Genome instability in Alzheimer disease

Hou, Yujun; Song, Hyundong; Croteau, Deborah L.; Akbari, Mansour; Bohr, Vilhelm A.

doi:10.1016/j.mad.2016.04.005

Cited by 120Alzheimer's disease research and treatmentsDNA Repair MechanismsDementia and Cognitive Impairment Research

Genome instability in Alzheimer disease

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Hou, Yujun, Song, Hyundong, Croteau, Deborah L., Akbari, Mansour, Bohr, Vilhelm A.·2017·Mechanisms of Ageing and Development

DOI 10.1016/j.mad.2016.04.005PMC PMC5195918

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Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disorder and the most common form of dementia. Autosomal dominant, familial AD (fAD) is very rare and caused by mutations in amyloid precursor protein (APP), presenilin-1 (PSEN-1), and presenilin-2 (PSEN-2) genes. The pathogenesis of sporadic AD (sAD) is more complex and variants of several genes are associated with an increased lifetime risk of AD. Nuclear and mitochondrial DNA integrity is pivotal during neuronal development, maintenance and function. DNA damage and alterations in cellular DNA repair capacity have been implicated in the aging process and in age-associated neurodegenerative diseases, including AD. These findings are supported by research using animal models of AD and in DNA repair deficient animal models. In recent years, novel mechanisms linking DNA damage to neuronal dysfunction have been identified and have led to the development of noninvasive treatment strategies. Further investigations into the molecular mechanisms connecting DNA damage to AD pathology may help to develop novel treatment strategies for this debilitating disease. Here we provide an overview of the role of genome instability and DNA repair deficiency in AD pathology and discuss research strategies that include genome instability as a component.

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While long-term potentiation is impaired in 3xTgAD mice, nicotinamide riboside restores LTP, correlating with improvements in learning and memory.
“While LTP is impaired in the 3xTgAD mice, NR restores LTP, correlating with improvements in learning and memory (Hou et al., 2017).”
From NAD+ in Brain Aging and Neurodegenerative Disorders (2019) · cites this paper as Hou et al., 2017

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Influence of Myocardial Infarction, Coronary Artery Bypass Surgery, and Stroke on Cognitive Impairment in Late Life 11This work has been supported by the National Institutes of Health, National Institute on Aging Contract 1-AG-4-2149, and National Heart, Lung, and Blood Institute Contract 1-HC-05102.
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Base excision DNA repair levels in mitochondrial lysates of Alzheimer's disease
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Lipopolysaccharide activates ERK–PARP-1–RelA pathway and promotes nuclear factor–κB transcription in murine macrophages
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Base excision repair in the mammalian brain: Implication for age related neurodegeneration
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Alzheimer's disease-associated polymorphisms in human OGG1 alter catalytic activity and sensitize cells to DNA damage
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Cytogenetic studies of familial and sporadic Alzheimer disease
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The Upstream Promoter of the β-Amyloid Precursor Protein Gene (APP) Shows Differential Patterns of Methylation in Human Brain
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Expression and Polymorphisms of Gene 8-Oxoguanine Glycosylase 1 and the Level of Oxidative DNA Damage in Peripheral Blood Lymphocytes of Patients with Alzheimer's Disease
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Contribution of defective mitophagy to the neurodegeneration in DNA repair-deficient disorders
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Single nucleotide polymorphisms in base-excision repair genes hOGG1, APE1 and XRCC1 do not alter risk of Alzheimer's disease
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Treatment of Alzheimer Disease
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The Arg194Trp polymorphism in DNA repair gene XRCC1 and the risk for sporadic late-onset Alzheimer's disease
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Mitochondrial DNA damage in a mouse model of Alzheimer's disease decreases amyloid beta plaque formation
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NAD+ metabolism: pathophysiologic mechanisms and therapeutic potential
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Alzheimer’s Disease Pathogenesis: Role of Autophagy and Mitophagy Focusing in Microglia
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Incorporation of a nucleoside analog maps genome repair sites in postmitotic human neurons
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Contributions of DNA Damage to Alzheimer’s Disease
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Natural Products in Alzheimer’s Disease Therapy: Would Old Therapeutic Approaches Fix the Broken Promise of Modern Medicines?
Habtemariam, S. (2019) · Molecules · doi:10.3390/molecules24081519 · Cited by 107 · see citing works
DNA Double-Strand Break Accumulation in Alzheimer’s Disease: Evidence from Experimental Models and Postmortem Human Brains
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Antioxidant Alternatives in the Treatment of Amyotrophic Lateral Sclerosis: A Comprehensive Review
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“Amyloid‐beta accumulation cycle” as a prevention and/or therapy target for Alzheimer's disease
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Ontogenetic and Pathogenetic Views on Somatic Chromosomal Mosaicism
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Interleukin33 deficiency causes tau abnormality and neurodegeneration with Alzheimer-like symptoms in aged mice
Carlock, C., Wu, J., Shim, J., Moreno‐González, I., Pitcher, M. R., Hicks, J., Suzuki, A., Iwata, J., Quevado, J., & Lou, Y. (2017) · Translational Psychiatry · doi:10.1038/tp.2017.142 · Cited by 59 · see citing works
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The Complex Mechanisms by Which Neurons Die Following DNA Damage in Neurodegenerative Diseases
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Role of primary aging hallmarks in Alzheimer´s disease
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Chromosome Instability, Aging and Brain Diseases
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The Phosphorylated Form of the Histone H2AX (γH2AX) in the Brain from Embryonic Life to Old Age
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An integrative machine-learning meta-analysis of high-throughput omics data identifies age-specific hallmarks of Alzheimer’s disease
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The potential role of COVID-19 in the induction of DNA damage
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Long genes are more frequently affected by somatic mutations and show reduced expression in Alzheimer's disease: Implications for disease etiology
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Molecular mechanisms underlying actions of certain long noncoding RNAs in Alzheimer’s disease
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The Hallmarks of Ageing in Microglia
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DNA repair gene OGG1 polymorphism and its relation with oxidative DNA damage in patients with Alzheimer’s disease
Dinçer, Y., Akkaya, Ç., Mutlu, T., Yavuzer, S., Erkol, G., Bozluolçay, M., & Güven, M. (2019) · Neuroscience Letters · doi:10.1016/j.neulet.2019.134362 · Cited by 30 · see citing works
Dynamic nature of somatic chromosomal mosaicism, genetic-environmental interactions and therapeutic opportunities in disease and aging
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GSK3‐ARC/Arg3.1 and GSK3‐Wnt signaling axes trigger amyloid‐β accumulation and neuroinflammation in middle‐aged Shugoshin 1 mice
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DNA Methylation in Genetic and Sporadic Forms of Neurodegeneration: Lessons from Alzheimer’s, Related Tauopathies and Genetic Tauopathies
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Some Molecular and Cellular Stress Mechanisms Associated with Neurodegenerative Diseases and Atherosclerosis
Sazonova, M. A., Sinyov, V. V., Ryzhkova, A. I., Sazonova, M. D., Kirichenko, T. V., Khotina, V. A., Khasanova, Z. B., Doroschuk, N. A., Karagodin, V. P., Orekhov, A. N., et al. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22020699 · Cited by 26 · see citing works
iPSC-derived cortical neurons to study sporadic Alzheimer disease: A transcriptome comparison with post-mortem brain samples
Verheijen, M. C. T., Krauskopf, J., Caiment, F., Nazaruk, M., Wen, Q. F., van Herwijnen, M. H. M., Hauser, D. A., Gajjar, M. K., Verfaillie, C. M., Vermeiren, Y., et al. (2021) · Toxicology Letters · doi:10.1016/j.toxlet.2021.12.009 · Cited by 25 · see citing works
Common aspects between glaucoma and brain neurodegeneration
Saccà, S. C., Paluan, F., Gandolfi, S., Manni, G., Cutolo, C. A., & Izzotti, A. (2020) · Mutation Research/Reviews in Mutation Research · doi:10.1016/j.mrrev.2020.108323 · Cited by 24 · see citing works
DNA Repair Inhibition Leads to Active Export of Repetitive Sequences to the Cytoplasm Triggering an Inflammatory Response
Song, X., Aw, J. T. M., Ma, F., Cheung, M. F., Leung, D., & Herrup, K. (2021) · The Journal of Neuroscience · doi:10.1523/jneurosci.0845-21.2021 · Cited by 23 · see citing works
Mitochondrial base excision repair positively correlates with longevity in the liver and heart of mammals
Gredilla, R., Sánchez-Román, I., Gómez, A. G., Lopez‐Torres, M., & Barja, G. (2020) · GeroScience · doi:10.1007/s11357-020-00158-4 · Cited by 22 · see citing works
The interplay between mitochondrial functionality and genome integrity in the prevention of human neurologic diseases
D’Errico, M., Parlanti, E., Pascucci, B., Filomeni, G., Mastroberardino, P. G., & Dogliotti, E. (2021) · Archives of Biochemistry and Biophysics · doi:10.1016/j.abb.2021.108977 · Cited by 20 · see citing works
Association of Caspase 3 Activation and H2AX γ Phosphorylation in the Aging Brain: Studies on Untreated and Irradiated Mice
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Causes 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
Alleviation of Photoreceptor Degeneration Based on Fullerenols in rd1 Mice by Reversing Mitochondrial Dysfunction via Modulation of Mitochondrial DNA Transcription and Leakage
Yang, J., Chen, X., Luodan, A., Gao, H., Zhao, M., Ge, L., Li, M., Cao, Y., Gong, Y. L., Gu, Z., et al. (2023) · Small · doi:10.1002/smll.202205998 · Cited by 20 · see citing works
Revealing the mechanisms of blood–brain barrier in chronic neurodegenerative disease: an opportunity for therapeutic intervention
Yu, S., Chen, X., Yang, T., Cheng, J., Liu, E., Jiang, L., Song, M., Shu, H., & Ma, Y. (2024) · Reviews in the Neurosciences · doi:10.1515/revneuro-2024-0040 · Cited by 23 · see citing works
Mitophagy pathways and Alzheimer's disease: From pathogenesis to treatment
Pan, X.-J., Misrani, A., Tabassum, S., & Yang, L. (2021) · Mitochondrion · doi:10.1016/j.mito.2021.04.007 · Cited by 18 · see citing works
Somatic mosaicism in the diseased brain
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Authors: Hou, Y., Song, H., Croteau, D. L., Akbari, M., & Bohr, V. A.
Affiliations: National Institute on Aging (US)
University of Copenhagen (DK)
National Institutes of Health (US)
Corresponding author: Bohr, Vilhelm A.
ORCID: Hou, Yujun
Croteau, Deborah L.
Akbari, Mansour
Bohr, Vilhelm A.
Venue: Mechanisms of Ageing and Development
Publisher: Elsevier BV
Published: 2017-01
Volume: 161
Issue: Pt A
Pages: 83-94
ISSN: 0047-6374 (ISSN-L)
DOI: 10.1016/j.mad.2016.04.005
PMC: PMC5195918
OpenAlex: W2342148852
Cited by: 120
References: 228
Citations by year: 2026: 6 · 2025: 5 · 2024: 15 · 2023: 14 · 2022: 9 · 2021: 24 · 2020: 19 · 2019: 16 · 2018: 4 · 2017: 6 · 2016: 1
FWCI: 1.06
Type: journal article
Language: en
Open access: green
researchprofiles.ku.dk
Licence: other-oa
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Mechanisms of Ageing and Development (publishedVersion)
PubMed (publishedVersion)
Research at the University of Copenhagen (University of Copenhagen) (publishedVersion, other-oa)
PubMed Central (acceptedVersion)
Funders: National Institutes of Health
National Institute on Aging (ZIAAG000723)
Topics: Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords: Alzheimer's disease, genomic instability, DNA repair deficiency, DNA damage, sporadic Alzheimer's disease, familial Alzheimer's disease, amyloid precursor protein, presenilin 1, presenilin 2, mitochondrial DNA integrity, neuronal dysfunction, aging, age-related neurodegeneration
MeSH terms: Alzheimer Disease, DNA Damage, DNA Repair, Humans, Mutation, Neurons, Amyloid beta-Protein Precursor, Genomic Instability, Presenilin-1

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