| Autor: |
Hickey JP; Department of Biomedical Sciences and Collaborative Specialization in Neuroscience Program, University of Guelph, Guelph, ON N1G 2W1, Canada., Collins AE; Department of Biomedical Sciences and Collaborative Specialization in Neuroscience Program, University of Guelph, Guelph, ON N1G 2W1, Canada., Nelson ML; Department of Biomedical Sciences and Collaborative Specialization in Neuroscience Program, University of Guelph, Guelph, ON N1G 2W1, Canada., Chen H; Department of Biomedical Sciences and Collaborative Specialization in Neuroscience Program, University of Guelph, Guelph, ON N1G 2W1, Canada., Kalisch BE; Department of Biomedical Sciences and Collaborative Specialization in Neuroscience Program, University of Guelph, Guelph, ON N1G 2W1, Canada. |
| Abstrakt: |
Alzheimer's disease (AD) is a progressive neurodegenerative disease and the most common form of dementia globally. Although the direct cause of AD remains under debate, neuroinflammation and oxidative stress are critical components in its pathogenesis and progression. As a result, compounds like cannabidiol (CBD) are being increasingly investigated for their ability to provide antioxidant and anti-inflammatory neuroprotection. CBD is the primary non-psychotropic phytocannabinoid derived from Cannabis sativa. It has been found to provide beneficial outcomes in a variety of medical conditions and is gaining increasing attention for its potential therapeutic application in AD. CBD is not psychoactive and its lipophilic nature allows its rapid distribution throughout the body, including across the blood-brain barrier (BBB). CBD also possesses anti-inflammatory, antioxidant, and neuroprotective properties, making it a viable candidate for AD treatment. This review outlines CBD's mechanism of action, the role of oxidative stress and neuroinflammation in AD, and the effectiveness and limitations of CBD in preclinical models of AD. |
