Scientists are reporting discovery in laboratory experiments of a previously unknown molecular mechanism in which the active ingredient in marijuana may slow the progression of Alzheimer's disease (AD).
Scripps Research Institute's Kim D. Janda and colleagues used laboratory experiments to show that delta-9-tetrahydrocannabinol (THC) preserves brain levels of the key neurotransmitter acetylcholine.
Existing medications for AD, including donepezil and tacrine, also relieve AD symptoms by inhibiting the enzyme, acetylcholinesterase, which breaks down acetylcholine.
THC does so by inhibiting an alternative site on acetylchlolinesterase and at lower concentrations, Janda's group reports in an article in the current (Oct. 2) issue of the ACS bimonthly journal, Molecular Pharmaceutics. Their experiments show that THC also prevents formation of the amyloid plaques that are a hallmark of AD and its damage to the brain.
"Our results provide a mechanism whereby the THC molecule can directly impact Alzheimer's disease pathology," they state. They also note that THC may provide a "drug lead" -- a model for developing new and more effective medications with more targeted effects on AD.
The researchers explain that such compounds "may provide an improved therapeutic for Alzheimer's disease, augmenting acetylcholine levels by preventing neurotransmitter degradation and reeducating amyloid beta aggregation, thereby simultaneously treating both the symptoms and progression of Alzheimer's disease."
The above post is reprinted from materials provided by American Chemical Society. Note: Materials may be edited for content and length.
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