Study: CB2 Receptor Activation a “Useful Therapeutic Approach for Alzheimer’s Disease”

Activation of the body’s CB2 receptors, something done naturally through the consumption of cannabis, is a “useful therapeutic approach for Alzheimer’s disease”, according to a new study.

“Alzheimer’s disease is a multifactorial disorder for which there is no disease-modifying treatment yet”, states the abstract of the study, published in the journal CNS Drugs. “CB2 receptors have emerged as a promising therapeutic target for Alzheimer’s disease because they are expressed in neuronal and glial cells and their activation has no psychoactive effects.”

The aim of this study was “to investigate whether activation of the CB2 receptor would restore the aberrant enhanced proliferative activity characteristic of immortalized lymphocytes from patients with late-onset Alzheimer’s disease. It is assumed that cell-cycle dysfunction occurs in both peripheral cells and neurons in patients with Alzheimer’s disease, contributing to the instigation of the disease.”

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Study: Cannabis has Therapeutic Potential in the Treatment of Alzheimer’s Disease

Cannabis may provide a potential treatment option for those with Alzheimer’s disease, states a new study published by the journal Neurochemical Research.

“Here we demonstrate for the first time that cannabidiol (CBD) acts to protect synaptic plasticity in an in vitro model of Alzheimer’s disease (AD)”, begins the study’s abstract. “The non-psycho active component of Cannabis sativa, CBD has previously been shown to protect against the neurotoxic effects of beta amyloid peptide (Aβ) in cell culture and cognitive behavioural models of neurodegeneration. Hippocampal long-term potentiation (LTP) is an activity dependent increase in synaptic efficacy often used to study cellular mechanisms related to memory.”

Here, researchers “show that acute application of soluble oligomeric beta amyloid peptide (Aβ1-42) associated with AD, attenuates LTP in the CA1 region of hippocampal slices from C57Bl/6 mice. Application of CBD alone did not alter LTP, however pre-treatment of slices with CBD rescued the Aβ1-42 mediated deficit in LTP.” The study found “that the neuroprotective effects of CBD were not reversed by WAY100635, ZM241385 or AM251, demonstrating a lack of involvement of 5HT1A, adenosine (A2A) or Cannabinoid type 1 (CB1) receptors respectively. However in the presence of the PPARγ antagonist GW9662 the neuroprotective effect of CBD was prevented.”

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