The putative contribution of cellular senescence to driving tauopathies.

Autor: Karabag D; Department for Neuroimmunology, Institute of Innate Immunity, Medical Faculty, University of Bonn, Bonn, Germany; German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany; University of Cologne, Faculty of Medicine and University Hospital Cologne, Cluster of Excellence Cellular Stress Response in Aging-associated Diseases (CECAD), Cologne, Germany., Heneka MT; Department for Neuroimmunology, Institute of Innate Immunity, Medical Faculty, University of Bonn, Bonn, Germany; German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany; Luxembourg Centre for Systems Biomedicine (LCSB), University of Luxembourg, Belvaux, Luxembourg; Division of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, MA, USA. Electronic address: michael.heneka@uni.lu., Ising C; University of Cologne, Faculty of Medicine and University Hospital Cologne, Cluster of Excellence Cellular Stress Response in Aging-associated Diseases (CECAD), Cologne, Germany. Electronic address: christina.ising@uk-koeln.de.
Jazyk: angličtina
Zdroj: Trends in immunology [Trends Immunol] 2024 Oct; Vol. 45 (10), pp. 837-848. Date of Electronic Publication: 2024 Sep 20.
DOI: 10.1016/j.it.2024.08.006
Abstrakt: During mammalian aging, senescent cells accumulate in the body. Recent evidence suggests that senescent cells potentially contribute to age-related neurodegenerative diseases in the central nervous system (CNS), including tauopathies such as Alzheimer's disease (AD). Senescent cells undergo irreversible cell cycle arrest and release an inflammatory 'senescence-associated secretory profile' (SASP), which can exert devastating effects on surrounding cells. Senescent markers and SASP factors have been detected in multiple brain cells in tauopathies, including microglia, astrocytes, and perhaps even post-mitotic neurons, possibly contributing to the initiation as well as progression of these diseases. Here, we discuss the implications of presenting a senescent phenotype in tauopathies and highlight a potential role for the NOD-like receptor protein 3 (NLRP3) inflammasome as a newfound mechanism implicated in senescence and SASP formation.
Competing Interests: Declaration of interests The authors declare no competing interests.
(Copyright © 2024 Elsevier Ltd. All rights reserved.)
Databáze: MEDLINE
Externí odkaz: