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Updated: Feb 13, 2026
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Evaluation of Motor Impairment in C. elegans Models of Amyotrophic Lateral Sclerosis
Published on: September 2, 2021
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DNA plasticity and damage in amyotrophic lateral sclerosis
Diane Penndorf1, Otto W Witte1, Alexandra Kretz1
1Hans Berger Department of Neurology, University Hospital Jena, Jena, Thuringia, Germany.
Neural Regeneration Research
|March 21, 2018
Summary
This review explores DNA damage and repair in amyotrophic lateral sclerosis (ALS) pathogenesis, highlighting genetic factors and unconventional DNA entities. Understanding these mechanisms is crucial for developing new ALS therapies beyond symptom management.
Area of Science:
- Neuroscience
- Genetics
- Molecular Biology
Background:
- Amyotrophic lateral sclerosis (ALS) presents complex pathophysiology due to clinical heterogeneity and diverse molecular/genetic factors.
- While genetic mutations are identified, the role of genome-wide DNA damage and repair in ALS initiation and progression remains unclear.
Purpose of the Study:
- To summarize current knowledge on DNA alterations and repair strategies in ALS.
- To discuss the potential involvement of unconventional DNA entities in ALS.
Main Methods:
- Review of existing literature on DNA damage, repair mechanisms, and genetic factors in ALS.
- Focus on specific genes like SOD1, FUS, TDP-43, and C9ORF72.
Main Results:
- Identified novel genetic factors contributing to both familial and sporadic ALS.
- Highlighted the incomplete understanding of DNA damage and repair's role in ALS.
- Discussed potential roles of transposable elements and extrachromosomal circular DNA.
Conclusions:
- Further research into DNA damage and repair in ALS is essential for a comprehensive understanding of the disease.
- This knowledge may pave the way for novel therapeutic strategies beyond current symptomatic treatments for ALS.
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