A group at UCD is researching the effects on electrical activity in their brain, which is related to learning, of a chemical found in high concentrations in Alzheimer’s disease patients.
The group — led by Dr Caroline Herron, Senior Lecturer at UCD’s School of Biomolecular and Biomedical Science — is investigating the effects of agents that interact with a set of cell surface proteins known as cannabinoid receptors. It has been shown that amyloids increase production of endocannabinoids.
The group hopes to determine if these agents could be used to protect normal brain cell function against the effects of amyloid beta protein. “Endogenous chemicals in the body act on cannabinoid receptors. These modulate activity in the brain at a low level,” said Dr Herron.
Local production of endocannabinoids in neuroinflammatory conditions is now considered a natural protective mechanism. CB2 receptors are present in a specific microglial cell type of the human cerebellum. These receptors are almost absent from the CNS in normal conditions but are up-regulated in glial cells under chronic neuroinflammatory stimuli – as has been described in AD. It is thought there is an increase in CB2 type microglial cells in inflammatory conditions.
In an attempt to understand the function of these receptors, a Spanish study tested their role in the process of A beta removal – currently considered as one of the most promising experimental approaches for the treatment of Alzheimer’s.
The Spanish team last year reported data indicating that the activation of CB2 receptors by low concentrations of the cannabinoid CB2 agonist JWH-015 resulted in the removal of pathological deposits with remarkable potency. Decreases of up to 64 per cent in plaque area were reported. The activation of cannabinoid CB2 receptors stimulates amyloid beta removal in situ and in vitro, it was found.
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