{"title":"DNA damage and repair in brain: relationship to aging","authors":"Kalluri Subba Rao , Lawrence A. Loeb","doi":"10.1016/0921-8734(92)90035-N","DOIUrl":null,"url":null,"abstract":"<div><p>The usefulness of conducting DNA damage and repair studies in a postmitotic tissue like brain is emphasized. We review studies that use brain as a tissue to test the validity of the DNA damage and repair hypothesis of aging. As far as the accumulation of age dependent DNA damage is concerned, the data appear to overwhelmingly support the hypothesis. However, attempts to demonstrate a decline in DNA repair capacity as a function of age are conflicting and equally divided. Possible reasons for this discrepancy are discussed. It is suggested that assessment of the repair capacity of neurons with respect to a specific type of damage in a specific gene might yield more definite answers regarding the role of DNA repair potential in the aging process and as a longevity assurance system.</p></div>","PeriodicalId":100937,"journal":{"name":"Mutation Research/DNAging","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"1992-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0921-8734(92)90035-N","citationCount":"47","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Mutation Research/DNAging","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/092187349290035N","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 47
Abstract
The usefulness of conducting DNA damage and repair studies in a postmitotic tissue like brain is emphasized. We review studies that use brain as a tissue to test the validity of the DNA damage and repair hypothesis of aging. As far as the accumulation of age dependent DNA damage is concerned, the data appear to overwhelmingly support the hypothesis. However, attempts to demonstrate a decline in DNA repair capacity as a function of age are conflicting and equally divided. Possible reasons for this discrepancy are discussed. It is suggested that assessment of the repair capacity of neurons with respect to a specific type of damage in a specific gene might yield more definite answers regarding the role of DNA repair potential in the aging process and as a longevity assurance system.
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