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CBD and other cannabinoids are currently under research scrutiny for possible pharmaceutical application in an even wider range of medical syndromes. One of them is vascular dementia. 

‘Vascular’ dementia refers to loss of brain function due to reduced blood perfusion into cerebral tissue. It is a common form of dementia. Inflammatory pathways have a major influence on this perfusion. All major cell types involved in the perfusion control pathways (i.e., smooth muscle, endothelium, neurons, astrocytes, pericytes, microglia, and leukocytes) are capable of synthesizing endocannabinoids, or expressing their target proteins. They function through the cannabinoid 1 and 2 receptors (or ‘CB1’ and ‘CB2’) or the transient receptor potential vanilloid type 1 ion channel. For this reason, the body’s endocannabinoid system, part of our onboard cell signaling network, can be expected to help regulate cerebral circulation. And because of this, cannabinoids may in time prove of value in therapeutic intervention. Presently, for vascular dementia, there is no satisfactory drug treatment. 

Experimental data since the 1990s supports the endocannabinoid system’s involvement in blood flow to the brain. The direct effect of cannabinoids on cerebral vessels is known to be vasodilation-mediated, at least in part, by CB1 receptors. Selective modulation of CB2 reduces memory impairment and infarct size during cerebral hypoperfusion and vascular dementia as well. 

Laboratory investigations of particular cannabinoid or cannabinoid-like agents are in their infancy, but have begun.

β-caryophyllene/hydroxypropyl-β-cyclodextrin, a natural sesquiterpene chemically similar to a cannabinoid, has improved cognitive deficits in animal models of vascular dementia through CB2. 

Paeoniflorin, a monoterpene glycoside, also acting on CB2, exhibits neuroprotective effects in the hippocampal CA1 region of vascular dementia, by modulating the M1/M2 subset polarization of microglia and macrophages. 

The synthetic cannabinoid receptor agonist WIN55,212-2 has demonstrated potential protective effects on cognitive dysfunction in another experimental model of vascular dementia as well. Its mechanism of action is associated with the suppression of autophagy and inflammation.