ArticleFrontiers in neuroscience2011
Reduced synchronization persistence in neural networks derived from atm-deficient mice.
Article in Frontiers in neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- Ataxia-telangiectasia mutated plays an important role in cerebellar integrity and functionality.Neural regeneration research · 2023Review
- Cellular functions of the protein kinase ATM and their relevance to human disease.Nature reviews. Molecular cell biology · 2021Review
- Inactive Atm abrogates DSB repair in mouse cerebellum more than does Atm loss, without causing a neurological phenotype.DNA repair · 2018Article
- Ataxia telangiectasia: a review.Orphanet journal of rare diseases · 2016Review
- Connecting Malfunctioning Glial Cells and Brain Degenerative Disorders.Genomics, proteomics & bioinformatics · 2016Review
- ATM and the epigenetics of the neuronal genome.Mechanisms of ageing and development · 2013Review
- The ATM protein kinase: regulating the cellular response to genotoxic stress, and more.Nature reviews. Molecular cell biology · 2013Review
- Malfunctioning DNA damage response (DDR) leads to the degeneration of nigro-striatal pathway in mouse brain.Journal of molecular neuroscience : MN · 2012Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Many neurodegenerative diseases are characterized by malfunction of the DNA damage response. Therefore, it is important to understand the connection between system level neural network behavior and DNA. Neural networks drawn from genetically engineered animals, interfaced with micro-electrode arrays allowed us to unveil connections between networks' system level activity properties and such genome instability. We discovered that Atm protein deficiency, which in humans leads to progressive motor impairment, leads to a reduced synchronization persistence compared to wild type synchronization, after chemically imposed DNA damage. Not only do these results suggest a role for DNA stability in neural network activity, they also establish an experimental paradigm for empirically determining the role a gene plays on the behavior of a neural network.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.