This receptor could be induced on demand throughout early inflammatory events and has been shown to be associated with attenuation of professional inflammatory cytokine production by microglia. Similar to macrophages at angiogenesis tumor peripheral sites, microglia can phagocytose and procedure antigens, and upon service make pro inflammatory facets like the cytokines IL IL 6, 1, and TNF. Pro inflammatory mediators released from microglia are cytotoxic and can also secondarily trigger astrocytes resulting in another induction of the appearance of inflammatory facets. The resulting storm of pro inflammatory mediators contributes to breakdown of the BBB and plays a vital role to promote influ into the CNS of immunocytes from peripheral non neuronal sites that also express CB2. Microglia are believed to play a major role in lots of neuropathogenic diseases and conditions such as Alzheimer s illness, Multiple Sclerosis, Amyotrophic Lateral Sclerosis, and HIV Encephalitis. AD is the most frequent neurodegenerative disorder that creates senile dementia. The defining neuropathologic options that come with the disease are the presence of extracellular neuritic amyloid plaques and intracellular neurofibrillary tangles in the brain. There is accelerated Lymph node neuroinflammation, neurofibrillary tangle development, and neuronal loss, as neurodegeneration advances. It’s been reported that cannabinoids can be neuroprotective in AD by inhibiting the activation of microglia caused by amyloid plaques consisting of extracellular aggregates of amyloid proteins. Recently, it had been mentioned that the CB2 and the CB1/CB2 agonist CP55940 agonist JWH 015 save and protect peripheral blood lymphocytes from A and H2O2 induced apoptosis by two alternative mechanisms. A receptor separate pathway was implicated through the demonstration of no oxidation in to consequently of cannabinoid inhibition of The generated H2O2 fluorescent rhodamine 123 while a receptordependent pathway was implicated through demonstration of p53 down-regulation and NF B activation involving CTEP phosphoinositide 3 kinase. These results suggested that cannabinoids have potential as neuroprotective materials in AD. Multiple sclerosis, also called disseminated sclerosis or encephalomyelitis spread, is a chronic, inflammatory demyelinating disease of the human CNS that primarily affects people. MS is characterized by T-cell mediated damage of the myelin sheath that covers axons, resulting in an inflammatory process that stimulates other immune cells to secrete pro inflammatory mediators and antibodies, breakdown of the BBB, activation of macrophages, and generation of cytotoxic proteins for example metalloproteinases. A somewhat greater density of CB2 immunoreactive microglia/macrophages is identified in affected regions of human MS post mortem spinal-cord.