and microglia,the resident macrophages of the brain, are involved along with blood-borne cells.
Although in the past glial activation in neuroinflammation has been considered detrimental to the brain in general, currently the reparative/ protective aspects are being recognized.
Cannabinoids, whether plant derived or endogenous affect different glial functions.
Importantly, glial cells are endowed with several, if not all, of the elements of the endocannabinoid system, and therefore are sensitive to cannabinoids and at the same time are a source of endocannabinoids.
There appears to be general agreement that cannabinoids reduce the synthesis, production, and release of cytotoxic molecules such as proinflammatory cytokines and nitric oxide.
On the other hand, these agents modify microglial cell migration in such a way that the result is usually beneficial in resolving neuroinflammation or limiting ensuing neurodegeneration.
-The Thought...
Cannabinoids can be neuroprotective via their immunomodulatory properties, which have been mainly attributed to CB2 receptors. These findings have relevance to anti-inflammatory effects of CB2 stimulation in brain. CB2-mediated regulation of this pathway could be very important for cannabinoid regulation of neuroinflammation.
-What Studies Saying
-In a 2012 review researchers concluded that "due to a myriad of neuro-protective, anti-neuro-inflammatory and anti-oxidant actions, cannabinoids have been cogitated as possible therapeutic agents for neurodegenerative disorders that combine inflammatory responses, as Alzheimer’s Disease (AD), Multiple Sclerosis (MS), Huntington and Parkinson Diseases.
Hyperactive microglia, a common feature of these neurodegenerative diseases, secrete a number of pro- and anti-inflammatory cytokines, chemokines, glutamate, prostanoids, neurotrophic factors, and a range of free radicals that provide a milieu for oxidative stress.
CBD has emerged as a promising strategy to treat inflammation that results from microglial hyperactivation, with no psychotropic side effects. Moreover, CBD has been shown to attenuate oxidative and nitrosative stress in several human disease models"
Also in a 2001 study bublished from Journals.plos.org researchers found that "CBD reduces Aβ-Induced Neuroinflammation and promotes Hippocampal Neurogenesis through PPARγ Involvement" Peroxisome proliferator-activated receptor-γ (PPARγ) has been reported to be involved in the etiology of pathological features of Alzheimer's disease
The results of this study showed that the blockade of PPARγ was able to significantly blunt CBD effects on reactive gliosis and subsequently on neuronal damage. Moreover, due to its interaction at PPARγ, CBD was observed to stimulate hippocampal neurogenesis. All these findings report the inescapable role of this receptor in mediating CBD actions
-In a study published in Neuroscience.com researchers found that
Cannabinoids are potent anti-inflammatory agents and they exert their effects through:
- Induction of apoptosis
- Lowering excitotoxicity
- Enhancing vasodilation
- Decreasing the release of pro-inflammatory mediators
- Inhibition of cell proliferation
- Suppression of cytokine production
- Induction of T-regulatory cells
In summary, the therapeutic use of cannabinoids in preclinical studies is being actively pursued in models of many neurodegenerative and mental diseases with great success. Nevertheless, the investigation of the effects of other important glial functions, and their consequences, should be extended in the near future.
For now, science aims to understand how cannabinoid compounds are associated with neuroinflammation and how cannabis-based medicine can help millions of patients worldwide. The development of safe, effective cannabis-based medicines must overcome the risk of adverse effects.
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