The hallmarks of aging in Ataxia-Telangiectasia

Julio Aguado*, Cecilia Gómez-Inclán, Hannah C. Leeson, Martin F. Lavin, Yosef Shiloh, Ernst J. Wolvetang

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

8 Scopus citations


Ataxia-telangiectasia (A-T) is caused by absence of the catalytic activity of ATM, a protein kinase that plays a central role in the DNA damage response, many branches of cellular metabolism, redox and mitochondrial homeostasis, and cell cycle regulation. A-T is a complex disorder characterized mainly by progressive cerebellar degeneration, immunodeficiency, radiation sensitivity, genome instability, and predisposition to cancer. It is increasingly recognized that the premature aging component of A-T is an important driver of this disease, and A-T is therefore an attractive model to study the aging process. This review outlines the current state of knowledge pertaining to the molecular and cellular signatures of aging in A-T and proposes how these new insights can guide novel therapeutic approaches for A-T.

Original languageEnglish
Article number101653
JournalAgeing Research Reviews
StatePublished - Aug 2022


FundersFunder number
BrAshA-T Foundation
Brisbane Children's Hospital Foundation- 50308
Israel Cancer Research Fund
A-T Children's Project
Dr. Miriam and Sheldon G. Adelson Medical Research Foundation
Australian Research CouncilDP210103401
National Health and Medical Research CouncilAPP2001408
United States-Israel Binational Science FoundationAPP1138795, APP1144806, APP1127976, APP1130168
University of QueenslandUQECR2058457


    • ATM
    • Aging
    • Ataxia-telangiectasia
    • Cellular senescence
    • DNA damage response
    • Mitochondrial dysfunction
    • Oxidative stress


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