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The role of ATM and DNA damage in neurons: upstream and downstream connections

Karl Herrup1, Jiali Li, Jianmin Chen

  • 1Division of Life Sciences, Hong Kong University of Science and Technology, Clear Water Bay, Kowloon, Hong Kong. herrup@biology.rutgers.edu

DNA Repair
|May 18, 2013
PubMed

Insights

The ataxia-telangiectasia mutated (ATM) protein kinase is crucial for DNA repair. Emerging evidence shows ATM also regulates vesicle dynamics and epigenetics, suggesting broader roles in neurodegeneration.

Area of Science:

  • Molecular Biology
  • Neuroscience
  • Genetics

Background:

  • The ataxia-telangiectasia mutated (ATM) protein kinase is primarily known for its role in DNA double-strand break repair.
  • However, neurological symptoms in ataxia-telangiectasia patients and ATM-mutant mice suggest functions beyond DNA repair in the nervous system.

Purpose of the Study:

  • To explore the broader functions of ATM in neuronal cells beyond DNA damage response.
  • To investigate ATM's potential involvement in neurodegenerative diseases.

Main Methods:

  • Review of existing literature on ATM function.
  • Analysis of ATM's role in vesicle dynamics and epigenetic regulation.
  • Examination of ATM levels in aging and neurodegenerative disease contexts.

Main Results:

  • ATM participates in vesicle dynamics and maintains histone modification patterns (epigenetic code).
  • Decreasing ATM levels with age correlate with neurodegenerative disease pathogenesis.
  • HDAC4 localization in Alzheimer's disease brains supports ATM's role in pathogenesis.

Conclusions:

  • ATM possesses multifaceted functions including DNA repair, vesicle dynamics, and epigenetic maintenance.
  • ATM signaling deficits may contribute to late-onset neurodegenerative diseases.
  • Understanding ATM's diverse roles is essential for comprehending ataxia-telangiectasia and related neurodegenerative conditions.
Keywords:
Alzheimer's diseaseAtaxia-telangiectasiaDNA damageEpigeneticsGlutamine

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