Glial decline and loss of homeostatic support rather than inflammation defines cognitive aging
Alexei Verkhratsky1
Natalia Lazareva2
Alexey Semyanov3
1.Faculty of Biology,Medicine and Health,The University of Manchester,Manchester,UK;Achucarro Center for Neuroscience,IKERBASQUE,Basque Foundation for Science,Bilbao,Department of Neurosciences,University of the Basque Country UPV/EHU and CIBERNED,Leioa,Spain;Sechenov First Moscow State Medical University,Moscow,Russia2.Sechenov First Moscow State Medical University,Moscow,Russia3.Sechenov First Moscow State Medical University,Moscow,Russia;Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry,Russian Academy of Sciences,Faculty of Biology,Moscow State University,Moscow,Russia
摘要：The preservation of cognitive longevity and arresting the pandemic of senile dementia engulfing the modern world is arguably the major challenge faced by biomedical research in the 21st century. Age is the leading risk factor for neurodegenerative diseases and vascular dementia, and yet there is a clear distinction between physiological and pathological brain aging; the former proceeds with cognitive abilities mainly preserved, whereas the latter is manifested with rapid cognitive decline. The cellular and molecular mechanisms of brain aging remain disputed, with numerous indications for metabolic and signaling alterations (Mattson and Arumugam, 2018).
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论文发表日期：2022-03-28
在线出版日期：2025-08-15（本平台首次上网日期，不代表文献的发表时间）
页数：2( 565-566 )