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Cannabidiol protects mouse hippocampal neurons from neurotoxicity induced by amyloid β-peptide 25 - 35

Alzheimer's disease (AD), the most prevalent form of dementia worldwide, is a significant health concern, according to the World Health Organization (WHO). The neuropathological diagnostic criteria for AD are based on the deposition of amyloid-β peptide (Aβ) and the formation of intracellular t...

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Bibliographic Details
Published in:Toxicology in vitro 2024-08, Vol.99, p.105880
Main Authors: Salgado, Karen Del Carmen Barboza, Nascimento, Rosiene Gomes de Freitas, Coelho, Pedro José Fernandes Nunes, Oliveira, Laser Antonio Machado, Nogueira, Katiane Oliveira Pinto Coelho
Format: Article
Language:English
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Summary:Alzheimer's disease (AD), the most prevalent form of dementia worldwide, is a significant health concern, according to the World Health Organization (WHO). The neuropathological diagnostic criteria for AD are based on the deposition of amyloid-β peptide (Aβ) and the formation of intracellular tau protein tangles. These proteins are associated with several overlapping neurodegenerative mechanisms, including oxidative stress, mitochondrial dysfunction, lipid peroxidation, reduced neuronal viability, and cell death. In this context, our study focuses on the potential therapeutic use of cannabidiol (CBD), a non-psychotropic cannabinoid with antioxidant and anti-inflammatory effects. We aim to evaluate CBD's neuroprotective role, particularly in protecting hippocampal neurons from Aβ -induced toxicity. Our findings indicate that CBD significantly improves cell viability and decreases levels of lipid peroxidation and oxidative stress. The results demonstrate that CBD possesses a robust potential to rescue cells from induced neurotoxicity through its antioxidant properties. Additionally, the neuroprotective effect of CBD may be associated with the modulation of the endocannabinoid system. These findings suggest that CBD could be a promising compound for adjuvant treatments in neurodegenerative processes triggered by amyloid-β peptide.
ISSN:1879-3177
DOI:10.1016/j.tiv.2024.105880