ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2019
Accumulation of Cytoplasmic DNA Due to ATM Deficiency Activates the Microglial Viral Response System with Neurotoxic Consequences.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06324877 (Single Arm Open-label Clinical Trial in Ataxia-telangiectasia to Test the Effects of Nicotinamide Riboside on Ataxia Scales, Immune Function, and Neurofilament Light Chain.), which is not on this map. Cited by 91 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Single Arm Open-label Clinical Trial in Ataxia-telangiectasia to Test the Effects of Nicotinamide Riboside on Ataxia Scales, Immune Function, and Neurofilament Light Chain.
Who cites it
91 citing papers in PubMed, 136 citations in OpenAlex.
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- NETSseq reveals inflammatory and aging mechanisms in distinct cell types, driving cerebellar decline in ataxia telangiectasia.Frontiers in neuroscience · 2025Article
- STING-mediated neuroinflammation: a therapeutic target in neurodegenerative diseases.Frontiers in aging neuroscience · 2025Review
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31 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 1 institution in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ATM (ataxia-telangiectasia mutated) is a PI3K-like kinase best known for its role in the DNA damage response (DDR), especially after double-strand breaks. Mutations in the ATM gene result in a condition known as ataxia-telangiectasia (A-T) that is characterized by cancer predisposition, radiosensitivity, neurodegeneration, sterility, and acquired immune deficiency. We show here that the innate immune system is not spared in A-T. ATM-deficient microglia adopt an active phenotype that includes the overproduction of proinflammatory cytokines that are toxic to cultured neurons and likely contribute to A-T neurodegeneration. Causatively, ATM dysfunction results in the accumulation of DNA in the cytoplasm of microglia as well as a variety of other cell types. In microglia, cytoplasmic DNA primes an antiviral response via the DNA sensor, STING (stimulator of interferon genes). The importance of this response pathway is supported by our finding that inhibition of STING blocks the overproduction of neurotoxic cytokines. Cytosolic DNA also activates the AIM2 (absent in melanoma 2) containing inflammasome and induces proteolytic processing of cytokine precursors such as pro-IL-1β. Our study furthers our understanding of neurodegeneration in A-T and highlights the role of cytosolic DNA in the innate immune response.
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