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Endocannabinoid signalling for GABAergic-microglia (mis) communication in the brain aging

In this article, the authors explore the role of endocannabinoid signaling in regulating communication between GABAergic neurons and microglia in the aging brain. They discuss how age-related neuroinflammation, caused by excessive activation of microglia and astrocytes, leads to cognitive decline and neurodegeneration. The authors suggest that the endocannabinoid system, which binds to cannabinoid receptors on neurons, microglia, astrocytes, and mitochondrial membranes, may modulate glial morphology and function to reduce the effects of age-related neuroinflammation and neurodegeneration.

The article also delves into the basic process of brain aging, which is a culmination of DNA damage, mitochondrial dysfunction, altered metabolism, altered intercellular communications, and overall cellular senescence. The authors emphasize the importance of the communication system between glial cells and neurons in regulating the immune response and the survival of neurons as individuals age.

The study of communications in the brain has been a long-researched field in neuroscience, with traditional research primarily focused on neuron-neuron and glia-glia communication mechanisms. However, recent research has begun to explore the communication system between the two dominant categories of cell types in the CNS: neuron and glia. This article discusses the existence of mixed communication styles between neurons and glia, which come as no surprise considering the previous identification of voltage-sensitive ion channels neurotransmitter receptors on glia.

The authors conclude that investigating the endocannabinoid receptors and ligands holds potential to help fully understand the communication system partly responsible for regulating glial cells that become dysfunctional. Although the system leaves many factors to be discovered, the information gathered and identified already could lead to the development of therapeutics to help reduce the effects of age-related neuroinflammation and neurodegeneration.



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