Retinoic acid isomers protect hippocampal neurons from amyloid-β induced neurodegeneration
Abstract
Attenuating amyloid-beta mediated neurodegeneration is of major therapeutic consideration in the potential treatment of Alzheimer disease. Previously, we found that a high dietary consumption of retinoic acid was associated with a reduced incidence of Alzheimer disease. Therefore, in this study, we investigated whether amyloid-beta mediated cell death in primary hippocampal neurons could be prevented by retinoic acid isomers. Our results suggest that retinoic acid isomers, including all-trans retinoic acid, 9-cis retinoic acid, and 13-cis retinoic acid, may play an important role in protecting neurons from amyloid-beta -induced cell death. Retinoic acid may therefore afford a novel therapeutic mechanism for the treatment and prevention of Alzheimer disease.
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The neuroprotective effect of ATRA seen in APP/PS1 mice is in line with a previous report showing protection against Aβ-induced injury of primary hippocampal neuronal cultures.
“The neuroprotective effect of ATRA seen in APP/PS1 mice is in line with a previous report showing protection against A-induced injury of primary hippocampal neuronal cultures (Sahin et al., 2005).”
From Retinoic Acid Attenuates β-Amyloid Deposition and Rescues Memory Deficits in an Alzheimer's Disease Transgenic Mouse Model (2008) · cites this paper as Sahin et al., 2005
ATRA overcomes the reduction in ChAT induced by Aβ peptides.
“and because ATRA overcomes the reduction in ChAT induced by A peptides (Sahin et al., 2005)”
From Retinoic Acid Attenuates β-Amyloid Deposition and Rescues Memory Deficits in an Alzheimer's Disease Transgenic Mouse Model (2008) · cites this paper as Sahin et al., 2005
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- Authors
- Sahin, M., Karaüzüm, S. B., Perry, G., Smith, M. A., & Alicigüzel, Y.
- Affiliations
- Akdeniz University (TR)
- Case Western Reserve University (US)
- Corresponding author
- Smith, Mark A.
- Venue
- Neurotoxicity Research
- Published
- 2005-01
- Volume
- 7
- Issue
- 3
- Pages
- 243-250
- ISSN
- 1029-8428 (ISSN-L)
- 1476-3524
- OpenAlex
- W2091587778
- Cited by
- 41
- References
- 59
- Citations by year
- 2026: 1 · 2023: 1 · 2022: 2 · 2021: 3 · 2019: 3 · 2018: 1 · 2017: 1 · 2016: 2 · 2015: 2 · 2014: 1 · 2013: 1 · 2012: 1
- FWCI
- 1.79
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Neurotoxicity Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Akdeniz Üniversitesi
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- retinoic acid isomers, amyloid-beta, neurodegeneration, hippocampal neurons, Alzheimer's disease, all-trans retinoic acid, 9-cis-retinoic acid, isotretinoin, neuronal cell death, neuroprotection
- MeSH terms
- Alitretinoin, Animals, Animals, Newborn, Cell Count, Dose-Response Relationship, Drug, Drug Interactions, Hippocampus, Nerve Degeneration, Neurons, Peptide Fragments, Tretinoin, Isotretinoin, Amyloid beta-Peptides, Cell Death, Protein Isoforms, Rats
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