A new cannabinoid may help protect the brain from aging

A large number of brain disorders associated with aging are characterized by progressive loss of neurons, including Alzheimer’s disease and Parkinson’s disease, among others. Over the past several decades, my laboratory’s research into the pathological mechanism underlying these diseases has documented the critical role of long-term brain inflammation.

Under normal circumstances, the inflammatory response in the brain is a protective process that promotes neuronal regeneration. However, when it persists for decades, inflammation predisposes certain regions of the brain to neurodegeneration. The brain cells that are primarily involved in this destructive inflammatory process are microglia.

The inflammatory response can be activated through various mechanisms, such as specific mutated genes, obesity, diabetes, environmental toxins, and pro-inflammatogens due to oxidative stress. Currently, there are no therapeutic agents that can effectively counteract the harmful effects of activated microglia or even slow down the progression of these disorders.

Until recently.

My research has shown that targeting the mechanisms underlying chronic neuroinflammation by stimulating cannabinoid receptors may be a promising strategy. Recent studies have shown that two endogenous fatty acids found in the brain, anandamide and palmitoylethanolamide (PEA), are also cannabinoids that can reduce the impact of many pathological mechanisms known to be involved in the neurodegenerative process. Anandamide is found naturally in cocoa powder and black truffles, while PEA is found in egg yolks, soybeans, and peanut oil. Both compounds can mimic the different effects of THC, the active ingredient found in cannabis products. Anandamide binds to both cannabinoid receptors and causes euphoria. In contrast, PEA does not bind well to cannabinoid receptors and has no apparent psychoactive effects.

The action of PEA is beneficial because it activates two important receptors that control inflammation and pain, PPAR-α and TRPV1. This dual action underlies the anti-inflammatory, antioxidant, analgesic and neuroprotective effects of PEA. PEA is safe for consumption; some countries have allowed the sale of products containing PEA as a dietary supplement for humans. The recommended dose is usually 600 to 1200 milligrams per day. A recent review of the PEA literature examined the clinical studies in defense of this dosing regimen.

Human and animal studies have provided strong neurobiological evidence for the therapeutic benefits of PEA, particularly in relation to changes observed in the brains of Alzheimer’s patients. PEA supplementation reduced brain inflammation, reduced amyloid protein expression, reduced the negative effects of tau protein in the hippocampus, and reduced glia activation. Taken together, these effects are associated with improved neuronal survival and widespread neuroprotection. The benefits of PEA were not limited to the brain; it also reduced the effects of inflammation in the gut and reduced oxidative stress levels throughout the body.

Consistent with this view of a beneficial role for PEA, brain levels of PEA have been shown to be reduced in patients with vascular dementia and Alzheimer’s disease. Analysis of previous studies on PEA also suggests that it has its maximum potential during the early stages of neurodegenerative diseases, stroke and Parkinson’s disease. The evidence gathered so far in animal and human studies is consistent with the recommendation to include dietary supplement PEA as a valuable adjunctive therapy to current approaches for the prevention and treatment of age-related neurogenerative diseases.

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