Cannabinoids in common dementia: an overview
The etiology of Alzheimer’s disease, Parkinson’s disease, and Huntington’s disease, the most common forms of dementia, is not completely known, but there are common molecular targets for therapy, including neuroinflammation, excitotoxicity, and mitochondrial dysfunction. In these processes the endogenous cannabinoid system is known to play a number of modulatory roles, notably involving up-regulation of CB2 receptors. 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 cannabidiol (CBD), an inverse agonist for several orphan receptor sites, is of 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.
Unfortunately, there is no evidence suggesting efficacy of cannabinoids in other forms of non-vascular dementia yet. One study, in 2007, suggested that CBD might appear useful in prion disease. This would have seemed good news to sufferers of Creutzfeldt-Jakob disease. That study did not clarify the mechanism involved, however, or identify what receptors were involved. Nor has CBD or any other cannabinoid since been shown to mitigate this or any prion-related disease.
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The foregoing is a report on trends and developments in the cannabinoid industry. No product described herein is intended to diagnose, treat, cure or prevent any disease or syndrome.