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


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


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


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