Universität zu Köln

Behfar, Q., Ramirez Zuniga, A. and Martino-Adami, Pamela V. (2022). Aging, Senescence, and Dementia. JPAD-J. Prev. Alzheimers Dis., 9 (3). S. 523 - 532. BASEL: SPRINGER BASEL AG. ISSN 2426-0266

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Abstract

The underlying processes occurring in aging are complex, involving numerous biological changes that result in chronic cellular stress and sterile inflammation. One of the main hallmarks of aging is senescence. While originally the term senescence was defined in the field of oncology further research has established that also microglia, astrocytes and neurons become senescent. Since age is the main risk factor for neurodegenerative diseases, it is reasonable to argue that cellular senescence might play a major role in Alzheimer's disease. Specific cellular changes seen during Alzheimer's disease are similar to those observed during senescence across all resident brain cell types. Furthermore, increased levels of senescence-associated secretory phenotype proteins such as IL-6, IGFBP, TGF-beta and MMP-10 have been found in both CSF and plasma samples from Alzheimer's disease patients. In addition, genome-wide association studies have identified that individuals with Alzheimer's disease carry a high burden of genetic risk variants in genes known to be involved in senescence, including ADAMIO, ADAMTS4, and BIN1. Thus, cellular senescence is emerging as a potential underlying disease process operating in Alzheimer's disease. This has also attracted more attention to exploiting cellular senescence as a therapeutic target. Several senolytic compounds with the capability to eliminate senescent cells have been examined in vivo and in vitro with notable results, suggesting they may provide a novel therapeutic avenue. Here, we reviewed the current knowledge of cellular senescence and discussed the evidence of senescence in various brain cell types and its putative role in inflammaging and neurodegenerative processes.

Item Type:	Journal Article
Creators:	Creators Email ORCID ORCID Put Code Behfar, Q. UNSPECIFIED UNSPECIFIED UNSPECIFIED Ramirez Zuniga, A. UNSPECIFIED UNSPECIFIED UNSPECIFIED Martino-Adami, Pamela V. UNSPECIFIED UNSPECIFIED UNSPECIFIED
URN:	urn:nbn:de:hbz:38-681096
DOI:	10.14283/jpad.2022.42
Journal or Publication Title:	JPAD-J. Prev. Alzheimers Dis.
Volume:	9
Number:	3
Page Range:	S. 523 - 532
Date:	2022
Publisher:	SPRINGER BASEL AG
Place of Publication:	BASEL
ISSN:	2426-0266
Language:	English
Faculty:	Unspecified
Divisions:	Unspecified
Subjects:	no entry
Uncontrolled Keywords:	Keywords Language BLOOD-BRAIN-BARRIER; UNFOLDED PROTEIN RESPONSE; CELLULAR SENESCENCE; ALZHEIMERS-DISEASE; DAMAGE RESPONSE; LIFE-SPAN; CELLS; MICROGLIA; AGE; INFLAMMATION Multiple languages Clinical Neurology Multiple languages
URI:	http://kups.ub.uni-koeln.de/id/eprint/68109