Publications by authors named "Emmanuelle Gruz-Gibelli"
Article Synopsis
- Researchers found that DNA double-strand breaks (DSBs) increased due to the A-amyloid peptide but decreased with all-trans retinoic acid (RA) in Alzheimer's disease models.
- In mutated cells, DSBs were less responsive to RA treatment compared to normal cells, indicating a malfunction in the repair mechanisms.
- The study suggests a compensatory neuroprotective mechanism involving increased BRCA1 and BARD1 proteins that helps lower DSB levels in mutant cells, which may be crucial in fighting Alzheimer's disease.
Article Synopsis
- The study explores the neuroprotective effects of all--retinoic acid (RA) against amyloid-beta (A)-induced DNA double-strand breaks (DSBs) in neuronal and astrocytic cell lines, and murine brain tissues.
- Findings indicate that RA not only repairs existing DSBs but also prevents their formation independent of other antioxidants like vitamin C, suggesting a complex mechanism involving PPAR/ and antiamyloidogenic proteins.
- The research concludes that RA operates through the RAR// and PPAR/ receptors, proposing that RA's pathways could serve as a preventive strategy to protect memory in Alzheimer’s disease and aging.
The amyloid-β peptide or Aβ is the key player in the amyloid-cascade hypothesis of Alzheimer's disease. Aβ appears to trigger cell death but also production of double-strand breaks (DSBs) in aging and Alzheimer's disease. All-trans retinoic acid (RA), a derivative of vitamin A, was already known for its neuroprotective effects against the amyloid cascade.
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