Cellular senescence in aging and age-related diseases: Implications for neurodegenerative diseases

Erin O. Wissler Gerdes, Yi Zhu, B. Melanie Weigand, Utkarsh Tripathi, Terence C. Burns, Tamar Tchkonia, James L. Kirkland

Research output: Chapter in Book/Report/Conference proceedingChapter

2 Scopus citations

Abstract

Aging is the major predictor for developing multiple neurodegenerative diseases, including Alzheimer's disease (AD) other dementias, and Parkinson's disease (PD). Senescent cells, which can drive aging phenotypes, accumulate at etiological sites of many age-related chronic diseases. These cells are resistant to apoptosis and can cause local and systemic dysfunction. Decreasing senescent cell abundance using senolytic drugs, agents that selectively target these cells, alleviates neurodegenerative diseases in preclinical models. In this review, we consider roles of senescent cells in neurodegenerative diseases and potential implications of senolytic agents as an innovative treatment.

Original languageEnglish (US)
Title of host publicationMetabolic and Bioenergetic Drivers of Neurodegenerative Disease
Subtitle of host publicationTreating neurodegenerative diseases as metabolic diseases
EditorsGrażyna Söderbom, Russell Esterline, Jan Oscarsson, Mark P. Mattson
PublisherAcademic Press Inc
Pages203-234
Number of pages32
ISBN (Print)9780128231210
DOIs
StatePublished - 2020

Publication series

NameInternational Review of Neurobiology
Volume155
ISSN (Print)0074-7742
ISSN (Electronic)2162-5514

Keywords

  • Alzheimer's disease
  • Cellular senescence
  • Dasatinib
  • Fisetin
  • Navitoclax
  • Parkinson's disease
  • Quercetin
  • Senescence-associated secretory phenotype
  • Senescent cell anti-apoptotic pathways
  • Senolytics

ASJC Scopus subject areas

  • Clinical Neurology
  • Cellular and Molecular Neuroscience

Fingerprint

Dive into the research topics of 'Cellular senescence in aging and age-related diseases: Implications for neurodegenerative diseases'. Together they form a unique fingerprint.

Cite this