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Cannabinoids remove plaque-forming Alzheimer's proteins from brain cells (2016)

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Why This Matters

This study highlights the potential of cannabinoids, specifically THC, to reduce amyloid beta proteins linked to Alzheimer's disease, offering a promising avenue for future therapeutics. As Alzheimer's continues to impact millions worldwide, these findings could lead to novel treatments that slow or prevent disease progression, benefiting both patients and the healthcare industry.

Key Takeaways

June 27, 2016

Cannabinoids remove plaque-forming Alzheimer’s proteins from brain cells

Preliminary lab studies at the Salk Institute find THC reduces beta amyloid proteins in human neurons

June 27, 2016

LA JOLLA–Salk Institute scientists have found preliminary evidence that tetrahydrocannabinol (THC) and other compounds found in marijuana can promote the cellular removal of amyloid beta, a toxic protein associated with Alzheimer’s disease.

While these exploratory studies were conducted in neurons grown in the laboratory, they may offer insight into the role of inflammation in Alzheimer’s disease and could provide clues to developing novel therapeutics for the disorder.

“Although other studies have offered evidence that cannabinoids might be neuroprotective against the symptoms of Alzheimer’s, we believe our study is the first to demonstrate that cannabinoids affect both inflammation and amyloid beta accumulation in nerve cells,” says Salk Professor David Schubert, the senior author of the paper.

Alzheimer’s disease is a progressive brain disorder that leads to memory loss and can seriously impair a person’s ability to carry out daily tasks. It affects more than five million Americans according to the National Institutes of Health, and is a leading cause of death. It is also the most common cause of dementia and its incidence is expected to triple during the next 50 years.

It has long been known that amyloid beta accumulates within the nerve cells of the aging brain well before the appearance of Alzheimer’s disease symptoms and plaques. Amyloid beta is a major component of the plaque deposits that are a hallmark of the disease. But the precise role of amyloid beta and the plaques it forms in the disease process remains unclear.

In a manuscript published in June 2016’s Aging and Mechanisms of Disease, the Salk team studied nerve cells altered to produce high levels of amyloid beta to mimic aspects of Alzheimer’s disease.

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