I hope everyone had a pleasant Labor Day, and has had a wonderful summer. I'll be finishing the summer's blogs with some more good news about the treatment of Alzheimer's disease.
Animal studies continue to be highly informative about approaches that can be taken in the treatment of Alzheimer's disease. A group of researchers at New York University (NYU) School of Medicine recently published an article in the Journal of Neuroscience, a journal which is widely respected for the quality of the research results it publishes. The NYU researchers investigated how a neurochemical, abnormal tau protein could be diminished in the brains of mice.
In a recent blog I discussed amyloid beta and its relationship to Alzheimer's disease. Both amyloid beta and abnormal tau protein are harmful to brain function and probably contribute to brain impairments in patients with Alzheimer's disease. Therefore, it would seem that ideal treatments for Alzheimer's disease would attempt to decrease both of these abnormal proteins.
In my previous blog on amyloid beta, I discussed one potential treatment approach being used to diminish abnormal amyloid in the brain. I particularly suggested that it might be possible to "drain" beta amyloid from the brain. However, beta amyloid, unlike abnormal tau protein, is present outside of brain cells, making it accessible to the "draining" approach. Abnormal tau protein is primarily within brain cells and cannot be treated in such a manner.
In order to overcome this obstacle, NYU researchers used an alternative method, one that involves the immune system. Mice with genetically increased tau protein and resulting functional brain impairments were given a tau protein vaccine. This vaccine was designed to attach to abnormal tau protein.
Typically the genetically abnormal mice have difficulty walking by about eight months. However, mice treated with the tau protein vaccine had maintained their ability to walk at the end of that time period. This preserved ability to walk corresponded to less abnormal tau protein in the brain. Therefore, it was concluded that tau vaccine, when given to genetically abnormal mice, could improve brain function by decreasing the abnormal tau protein.
This research study shows the continued growth in our knowledge, understanding, and ability to approach the scientific aspects of Alzheimer's disease. As I have indicated previously, there are multiple levels of study necessary for a potential treatment to become an actual treatment implemented by doctors. Animal studies, such as the study summarized here, are exciting and are an indication of the tremendous growth in our knowledge about Alzheimer's disease.