Alzheimer's disease, a brain disorder that causes memory loss and dementia, is one of the leading causes of death and affects more than five million Americans according to the National Institute of Health. With its incidence being projected to triple during the next 50 years, Alzheimer's disease is an increasing problem with the elderly population.

Amyloid Beta: What is it?

The deterioration of the brain that occurs during Alzheimer's is due to the plaques from amyloid beta proteins clumping together. Amyloid beta is an indicator of Alzheimer's disease, present within the brain prior to Alzheimer's disease patients becoming symptomatic of the disease. Small clumps of this protein can block synapsing between neuronal cells.

Brain inflammation is also commonplace with Alzheimer's disease. In June 2016's Aging and Mechanisms of Disease, members of the Salk Institute team studied nerve cells altered to produce higher levels of the amyloid beta protein in order to mimic the conditions found in Alzheimer's. High levels of the protein are associated with cellular inflammation and higher rates of neuronal death. Previously, it was thought that the inflammation occurred from immune cells, but an uncanny discovery proved otherwise the amyloid beta proteins instead are the cause of inflammatory effects within the brain.

Endocannabinoids, THC, and Neuronal Survival

Endocannibonoids are a class of lipid molecules produced naturally by the body utilized in intercellular signaling within the brain. The discovery of endocannabinoids came from research on an Alzheimer's drug candidate, J147, of which removed amyloid beta from neurons and reduced inflammatory effects. Endocannabinoids were discovered to be involved in the reduction of amyloid beta proteins and reduction of inflammation. In previous research done on Alzheimer's disease, physical activity has been proven to increase the production of endocannibonoids, and thus exercise is recommended to slow the progression of Alzheimer's. Tetrahydrocannabinol (THC), the psychoactive component of marijuana, is similar to endocannibonoids in molecular structure and thus have similar effects in the brain.

In the Salk Institute study spearheaded by Salk Professor David Schubert, amyloid beta protein levels exposed to high levels of THC compounds reduced the amyloid beta protein levels as well as eliminated the inflammatory response from neuronal cells caused by the protein. The reduction of amyloid beta protein levels and inflammation allow the neurons to survive. THC-like compounds, like endocannibinoids, may be involved in protecting neuronal cells from death.

Future Treatments Involving THC

With other studies offering evidence that cannabinoids might be neuroprotective against Alzheimer's disease, the possibilities of cannabinoids used for medicinal purposes has increased to encompass this virulent disease. THC compounds used for treatment in Alzheimer's cases still require clinical trials, but hold much promise for the future of Alzheimer's treatments.

Reference
  1. Antonio Currais, Oswald Quehenberger, Aaron M Armando, Daniel Daugherty, Pam Maher, David Schubert. Amyloid proteotoxicity initiates an inflammatory response blocked by cannabinoids. npj Aging and Mechanisms of Disease, 2016; 2: 16012 DOI: 10.1038/npjamd.2016.12
  2. Salk Institute. (2016, June 29). Cannabinoids remove plaque-forming Alzheimer's proteins from brain cells. ScienceDaily. Retrieved July 13, 2016 from www.sciencedaily.com/releases/2016/06/160629095609.htm

See the other latest Alzheimer's Research in the links below:

Keys to Fighting Alzheimer's: 2016 Research

Dementia Research Article (2016)

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