The cannabinoid system is represented by two principal receptor subtypes,
termed CB1 and CB2, along with several endogenous ligands. In the central nervous
system it is involved in several processes. CB1 receptors are mainly expressed by neurons
and their activation is primarily implicated in psychotropic and motor effects of
cannabinoids. CB2 receptors are expressed by glial cells and are thought to participate in
regulation of neuroimmune reactions. This review aims to highlight several reported
properties of cannabinoids that could be used to inhibit the adverse neuroinflammatory
processes contributing to Parkinson’s disease and possibly other neurodegenerative
disorders. These include anti-oxidant properties of phytocannabinoids and synthetic
cannabinoids as well as hypothermic and antipyretic effects. However, cannabinoids may
also trigger signaling cascades leading to impaired mitochondrial enzyme activity, reduced
mitochondrial biogenesis, and increased oxidative stress, all of which could contribute to
neurotoxicity. Therefore, further pharmacological studies are needed to allow rational
design of new cannabinoid-based drugs lacking detrimental in vivo effects.
Keywords: Alzheimer’s disease, cannabinoid receptors, cannabidiol,
endocannabinoids, fever, marijuana, microglia, mitochondrial dysfunction,
neurodegeneration, neuroinflammation, oxidative stress, Parkinson’s disease,
Δ9-tetrahydrocannabinol (THC), thermoregulation.
