This article provides a rather detailed explanation for the multiple beneficial aspects of cannabinoids for the treatment of Alzheimer's disease. Again there are other aromatic plants that accomplish the same thing for those who don't want to try medical marijuana. Among the more important findings are the role of cannabinoids as antioxidants, at reducing inflammation, and in inhibiting mitochondrial dysfunction.
Front. Pharmacol., 05 March 2014 | doi: 10.3389/fphar.2014.00037
Cannabinoids for treatment of Alzheimer’s disease: moving toward the clinic
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Conclusions and Therapeutic Implications Considering the numerous complex pathological mechanisms involved in the progression of AD, treatments targeting a single causal or modifying factor offer limited benefit. Cannabinoids, however, exhibit pleiotropic activity, targeting in parallel several processes that play key roles in AD, including Aβ and tau aberrant processing, neuroinflammation, excitotoxicity, mitochondrial dysfunction, and oxidative stress. Cannabinoids improve behavioral disturbances, as well.
The main concerns regarding the use of cannabis derivatives in medicine are related with the psychoactivity of some cannabinoids, especially Δ9-THC, which may disrupt short-term memory, working memory, and attention skills mainly acting through CB1 receptors, as well as with the potential Δ9-THC dependence occurring after long-term use. However, the therapeutic effects of cannabinoids must be clearly dissociated from the risks of abuse and addiction linked to the recreational use of cannabis derivatives. First, the CB1 agonists with potential psychoactivity used in experimental models to demonstrate the therapeutic properties were administered at doses substantially lower than those producing psychoactive effects and cannabis dependence (Maldonado et al., 2011). Second, the preferred therapeutic cannabinoid combination includes CBD, which is known to mitigate the negative consequences on cognition of Δ9-THC administration (Fadda et al., 2004), and therefore insure the avoidance of such undesirable effects. Finally, the brain context in healthy subjects consuming cannabis enriched in Δ9-THC for recreational purposes is completely different from that of AD patients subjected to very determined combinations of cannabinoid species, in terms of ECS [endogenous cannabinoid system] organization and neuronal signaling. In conclusion, in light of the polyvalent properties for the treatment of AD and the limited side effects exhibited by these compounds, progress toward a clinical trial to test the capacity of cannabinoids to curb this neurodegenerative disease seems to be fully justified.