Neural Regeneration Research ›› 2022, Vol. 17 ›› Issue (3): 565-566.doi: 10.4103/1673-5374.320979

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Glial decline and loss of homeostatic support rather than inflammation defines cognitive aging

Alexei Verkhratsky*, Natalia Lazareva, Alexey Semyanov   

  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 (Verkhratsky A)
    Sechenov First Moscow State Medical University, Moscow, Russia (Verkhratsky A, Lazareva N, Semyanov A)
    Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences, Faculty of Biology, Moscow State University, Moscow, Russia (Semyanov A)
  • Online:2022-03-15 Published:2021-10-15
  • Contact: Alexei Verkhratsky, PhD, Alexej.Verkhratsky@manchester.ac.uk.
  • Supported by:
    The work of AS was supported by the Russian Science Foundation, No. 20-14-00241.

Abstract: 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). Chronic neuroinflammation in particular, is frequently considered as a universal attribute of aging (Di Benedetto et al., 2017), with brain aging being but a part of “inflammageing” (Franceschi et al., 2007) embracing the whole organism. This view, however, needs to be corroborated, particularly considering that the concept of neuroinflammation is not clearly defined. Reactive gliosis (astrogliosis or microgliosis, and possibly reactivity of oligodendrocyte precursor cells also known as NG-2 glia) is frequently regarded as the ultimate sign of neuroinflammation and aging is generally believed to be associated with progressive increase in glial reactivity. Experimental evidence for the predominance of reactive glia in the old brain is however controversial; instead, the age-dependent glial morphofunctional decline may present more accurate description of brain aging.