Cited by 110DNA Repair MechanismsNeurogenesis and neuroplasticity mechanismsCRISPR and Genetic Engineering

DNA double-strand breaks as drivers of neural genomic change, function, and disease

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Alt, Frederick W., Schwer, Bjoern·2018·DNA Repair

Abstract

Early work from about two decades ago implicated DNA double-strand break (DSB) formation and repair in neuronal development. Findings emerging from recent studies of DSBs in proliferating neural progenitors and in mature, non-dividing neurons suggest important roles of DSBs in brain physiology, aging, cancer, psychiatric and neurodegenerative disorders. We provide an overview of some findings and speculate on what may lie ahead.

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Crossref · 10.1016/j.dnarep.2018.08.019

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  • DSBs play important roles in cell physiology, including T-cell receptor and antibody diversity, chromosomal recombination during meiosis, and immediate early gene expression in neurons.

    “DSBs are required for T‐cell receptor and antibody diversity, chromosomal recombination during meiosis, and in the case of neurons, assist in the expression of immediate early genes”

    From Mechanisms of DNA damage-mediated neurotoxicity in neurodegenerative disease (2022) · cites this paper as Alt & Schwer, 2018

  • Somatic mutations induced by erroneous DNA damage repair or transposable elements are a common feature of neural development, giving rise to neuron diversity through genomic mosaicism.

    “somatic mutations induced by erroneous DNA damage repair or transposable elements are a common feature of neural development, giving rise to neuron diversity through genomic mosaicism”

    From Mechanisms of DNA damage-mediated neurotoxicity in neurodegenerative disease (2022) · cites this paper as Alt & Schwer, 2018

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Authors
Alt, F. W., & Schwer, B.
Affiliations
  • Boston Children's Hospital (US)
  • University of California, San Francisco (US)
Corresponding author
  • Alt, Frederick W.
  • Schwer, Bjoern
Venue
DNA Repair
Publisher
Elsevier BV
Published
2018-11
Volume
71
Pages
158-163
ISSN
  • 1568-7856 (ISSN-L)
  • 1568-7864
OpenAlex
W2888718906
Cited by
110
References
75
Citations by year
2026: 6 · 2025: 12 · 2024: 14 · 2023: 13 · 2022: 18 · 2021: 12 · 2020: 22 · 2019: 11 · 2018: 2
FWCI
1.15
Type
journal article
Language
en
Open access
Locations
  • DNA repair (acceptedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
  • eScholarship (California Digital Library) (submittedVersion)
Funders
  • National Institute on Aging
  • National Institutes of Health (AG043630)
  • University of California, San Francisco
  • Howard Hughes Medical Institute
  • Shurl and Kay Curci Foundation
  • Andrew McDonough B+ Foundation
  • American Cancer Society
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
  • Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › CRISPR and Genetic Engineering
Keywords
DNA double-strand breaks, neurons, neural progenitor cells, neuronal development, brain aging, neurodegenerative diseases, mental illness, brain cancer
MeSH terms
Animals, DNA, DNA Repair, Humans, Genome, Genomic Instability, DNA Breaks, Double-Stranded, Neurogenesis, Neural Stem Cells

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