A study conducted by the Stanford University's School of Medicine suggested beta-amyloid may lead to the beneficial action of endocannabinoids (brain's internal version of marijuana and hashish) being blocked in the brain. Beta-amyloid, suspected to play a key role in Azheimer's, forms the clumps choking the brains of Alzheimer patients impairing learning and memory.
Dr. Daniel Madison, associate professor of molecular and cellular physiology, cited, "It would be wildly off the mark to assume that, just because A-beta interferes with a valuable neurophysiological process mediated by endocannabinoids, smoking pot would be a great way to counter or prevent A-beta's nefarious effects on memory and learning ability. Smoking or ingesting marijuana results in long-acting inhibition of interneurons by the herb's active chemical, tetrahydrocannabinol. That is vastly different from short-acting endocannabinoid bursts precisely timed to occur only when a signal is truly worthy of attention. Endocannabinoids in the brain are very transient and act only when important inputs come in. Exposure to marijuana over minutes or hours is different: More like enhancing everything indiscriminately, so you lose the filtering effect. It's like listening to five radio stations at once."
In the early stages of Alzheimer's, the memory begins to fade. Madison and his team analyzed beta-amyloid's effects on a structure known as hippocampus, which is a brain structured shape like a sea horse.
It was noted the first area of brain damage in those affected by Alzheimer's is the hippocampus.
Madison explained, "The hippocampus tells us where we are in space at any given time. It also processes new experiences so that our memories of them can be stored in other parts of the brain. It's the filing secretary, not the filing cabinet."
The professor said pinning down the molecular details behind amyloid-beta's effect on endocannabinoids could pave the way to new Alzheimer's drugs.