William B. Miller Jr , František Baluška , Arthur S. Reber , Predrag Slijepčević
{"title":"Why death and aging ? All memories are imperfect","authors":"William B. Miller Jr , František Baluška , Arthur S. Reber , Predrag Slijepčević","doi":"10.1016/j.pbiomolbio.2024.02.001","DOIUrl":null,"url":null,"abstract":"<div><p>Recent papers have emphasized the primary role of cellular information management in biological and evolutionary development. In this framework, intelligent cells collectively measure environmental cues to improve informational validity to support natural cellular engineering as collaborative decision-making and problem-solving in confrontation with environmental stresses. These collective actions are crucially dependent on cell-based memories as acquired patterns of response to environmental stressors. Notably, in a cellular self-referential framework, all biological information is ambiguous. This conditional requirement imposes a previously unexplored derivative. All cellular memories are imperfect. From this atypical background, a novel theory of aging and death is proposed. Since cellular decision-making is memory-dependent and biology is a continuous natural learning system, the accumulation of previously acquired imperfect memories eventually overwhelms the flexibility cells require to react adroitly to contemporaneous stresses to support continued cellular homeorhetic balance. The result is a gradual breakdown of the critical ability to efficiently measure environmental information and effect cell-cell communication. This age-dependent accretion governs senescence, ultimately ending in death as an organism-wide failure of cellular networking. This approach to aging and death is compatible with all prior theories. Each earlier approach illuminates different pertinent cellular signatures of this ongoing, obliged, living process.</p></div>","PeriodicalId":3,"journal":{"name":"ACS Applied Electronic Materials","volume":null,"pages":null},"PeriodicalIF":4.3000,"publicationDate":"2024-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"ACS Applied Electronic Materials","FirstCategoryId":"99","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0079610724000178","RegionNum":3,"RegionCategory":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"ENGINEERING, ELECTRICAL & ELECTRONIC","Score":null,"Total":0}
引用次数: 0
Abstract
Recent papers have emphasized the primary role of cellular information management in biological and evolutionary development. In this framework, intelligent cells collectively measure environmental cues to improve informational validity to support natural cellular engineering as collaborative decision-making and problem-solving in confrontation with environmental stresses. These collective actions are crucially dependent on cell-based memories as acquired patterns of response to environmental stressors. Notably, in a cellular self-referential framework, all biological information is ambiguous. This conditional requirement imposes a previously unexplored derivative. All cellular memories are imperfect. From this atypical background, a novel theory of aging and death is proposed. Since cellular decision-making is memory-dependent and biology is a continuous natural learning system, the accumulation of previously acquired imperfect memories eventually overwhelms the flexibility cells require to react adroitly to contemporaneous stresses to support continued cellular homeorhetic balance. The result is a gradual breakdown of the critical ability to efficiently measure environmental information and effect cell-cell communication. This age-dependent accretion governs senescence, ultimately ending in death as an organism-wide failure of cellular networking. This approach to aging and death is compatible with all prior theories. Each earlier approach illuminates different pertinent cellular signatures of this ongoing, obliged, living process.