Cannabinoids in common dementia: a research overview

by Duncan Fisher

August 22, 2022 - 2 min read

There are numerous forms of dementia. The common ones, and what most of us mean by ‘dementia’, are Alzheimer’s disease, Parkinson’s disease, and Huntington’s disease. What causes them is not completely known, but there are known molecular mechanisms that may be of use in future therapy. These include neuroinflammation, excitotoxicity, and mitochondrial dysfunction. And in these processes the endogenous cannabinoid system, part of our onboard neurological cell-signaling network, is known to play a number of roles, notably involving up-regulation of CB2 receptors. ‘CB1’ and ‘CB2’ refer to the two known binding sites of cannabinoid molecules. This will be an area of ever-greater research importance as lifespan increases in the developed world. Practical trials of cannabinoids in dementia so far are inconclusive, but they are turning up data that warrant more investigation. Cannabidiol (CBD), an inverse agonist for several orphan receptor sites, is of particular interest at the moment. 

Against Alzheimer’s disease, CBD possesses known neuroprotective, antioxidant, and anti-inflammatory properties, and it reduces amyloid plaque production (as does at least one synthetic cannabinoid) and tau hyperphosphorylation in vitro. Long-term treatment with CBD prevents the development of memory deficits in Alzheimer’s disease transgenic mice.  Anandamide is another endocannabinoid that appears neuroprotective in Alzheimer’s disease.

In Parkinson’s disease as well, cannabinoids are emerging as putative therapies, at least in motor deficits. Of promise latterly are CBD, its synthetic isomer Abn-CBD, the sesquiterpene beta-Caryophyllene, AM1241, a CB2 agonist that promotes neuronal regeneration in mice, and VCE-003.2, a cannabigerol quinone derivative with anti-inflammatory properties. Studies are yet limited, but do appear to warrant further exploration.

Recent study of cannabinoids in Huntington’s disease show improvement in motor symptoms and also in behaviour. Cannabinoids may reduce hyperkinesia by activating vanilloid TRPV(1) receptors, and they may delay disease progression by protecting striatal neurons from early death.

Experimental data since the 1990’s suggests that cannabinoids also function in cerebral vasodilation. Thus, CB2 modulators work against biochemical alterations and brain damage in at least one model of vascular dementia. Through this pathway, in rats, a beta-Caryophellene complex has been observed to improve cognitive deficits. 

Finally, evidence is present that there is even a role for endocannabinoids in HIV-associated dementia. Activation of CB2 receptors clearly inhibits HIV-1 envelope glycoprotein gp120-induced synapse loss.

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