Alzheimer’s disease is a neurodegenerative condition that affects over 6 million Americans. The vast majority of those who develop Alzheimer’s disease are over 65 years of age and as many as 1 in 9 (11.3%) from this age group are currently living with the disease. Early symptoms include memory loss and language problems. In time, these symptoms grow increasingly severe. As the disease progresses and more nerve cells in the central nervous system are affected, patients lose the ability to carry out basic bodily functions and cease to be able to care for themselves. At this time, there is no cure.
There is some good news, however. In the past decade or so, researchers have come to recognize that one of the signatures of Alzheimer’s disease is a buildup of beta-amyloid proteins that first form tiny fibers (fibrils) before going on to make plaque. Though the exact sequencing of events is still unknown, there is a positive association between more severe neuron damage and the increasing presence of such plaques, as well as tangles of molecules known as tau proteins. This suggests that amyloid-beta plaque and tau tangles become toxic to neurons once they hit a critical point, and this neuron damage is what leads to the symptoms associated with Alzheimer’s disease.
For years, researchers have reasoned that finding a molecule that can successfully disrupt the buildup of beta-amyloid plaques in the brain could mean that they can arrest the development of the disease. A recently published paper in the Journal of Molecular Graphics and Modeling by two researchers out of the Indian Institute of Technology Guwahati, Pavan Krishna Kanchi and Ashok Kumar Dasmahapatra, have found that tetrahydrocannabinol (THC) appears to do just that by interfering with the creation of beta-amyloid protofibrils. Their study found the specific means through which THC bonds with the protofibrils, thereby inhibiting aggregation and preventing the formation of fibrils, and then plaques.
More research is needed to see how effective THC is at binding to protofibrils in vivo, but the team’s paper is certainly a cause for optimism.
The Journal of Molecular Graphics and Modelling has more.