There is a form of neurocognitive impairment that can come with HIV infection. Based on findings that synthetic cannabinoids inhibit HIV-1 expression in human microglia and suppress production of inflammatory mediators such as nitric oxide in human astrocytes, all buttressed by a substantial literature demonstrating neuroprotective properties of cannabinoids in other neural systems, the concept of synthetic cannabinoids as potential therapeutic agents in this HIV-related neuropathogenesis is beginning to emerge as a possibility.
A role for the endocannabinoid system in HIV symptomology, as part of the body’s onboard cell-signaling network, has been verified by experimental data. Cannabinoids inhibit HIV-1 Gp120-mediated insults in brain microvascular endothelial cells.
It is at cannabinoid receptor site 2 (‘CB2’) that this seems to be mediated. Gp120 is an HIV-1 glycoprotein, that induces apoptosis in neurons, and is involved in the pathogenesis of HIV-associated dementia, where it appears to inhibit proliferation of adult neural progenitor cells. Activation of CB2 receptors ameliorates gp120-induced synapse loss. The CB2 synthetic agonist AM1241 enhances neurogenesis in GFAP/Gp120 transgenic mice displaying deficits in neurogenesis.
In other studies, brains of hu-PBL/HIVE mice show microglial activation and increased expression of CB2, but not CB1 or GPR55. (‘HIVE’ refers to HIV-related encephalitis, a general term for disease-induced nerve damage.) Gp1a substantially reduces infiltration of human cells into mouse brains and reduces HLA DQ activation as well. And Gp1a has been shown to down-modulate CCR5 expression in human cells in the spleen with an increase in Fas ligand expression.
Interestingly, expression of CB1 has also been noted to increase in glia of HIVE brains, though not as much as CB2 in white matter. Morphologically, CB1 clearly is present in HIVE brain neurons, and both CB1 and CB2 are present in meningeal macrophages and subpial glia in all brains. In HIVE, CB1 has been found in white matter microglia and perivascular cells, while CB2 has been shown to proliferate in microglia, astrocytes and perivascular macrophages. Double immunofluorescence with cell-specific markers and immunoblots on primary cultured microglia and astrocytes substantiates localization of the cannabinoid receptors in the glia, and the specificity of the antibodies as well. Cannabinoid receptor expression occurs broadly in HIVE brains, in other words, and this may have ramifications for the potential use of cannabinoid ligands in HIV-infected patients with dementia.
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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.
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