Intriguing New Insight into Cause of Alzheimer's

Contributed by: Dennis Fortier, President, Medical Care Corporation

As the experts in the field readily acknowledge, they really don't understand Alzheimer's disease very well.  A new hypothesis, based on a recent publication in the Journal of Neuroscience, suggests that previous views and treatment approaches might be aiming at the wrong target.

The dominant theory (the amyloid hypothesis) is that excess accumulation of beta-amyloid, a naturally occurring protein in the brain, aggregates into toxic plaques that disrupt cell function and leads to cognitive decline.  Based on the new research, it is plausible that beta-amyloid is in fact the main culprit, but that it does its damage inside the brain cells, prior to breaking free and accumulating into plaques.

Some of the general press on these findings have described the science as a complete contradiction of the amyloid-hypothesis.  In reality however, it is fairly consistent with one important difference.

The new insight is that beta-amyloid might be causing harm earlier in the biological process than previously believed.  This study suggests that once the beta-amyloid has been dispensed from brain cells and clumps together into a plaque, the damage has already been done. Previously, it has been theorized that the formation of the plaque is the beginning of a toxic biological process.

The implications for treatment are that we should be looking to reduce the presence of beta-amyloid inside the cells, as opposed to clearing it away later, once it has aggregated into a plaque. Fortunately, two of the most promising agents in the FDA pipeline, Bapineuzumab and Solanezumab, are both antibodies that bind to beta-amyloid and clear it away through the natural immune function. It is hoped that one or both of these agents might function at the early, biological stage suggested by this new insight.


  1. so it's true, I heard this same history in many other sites, but I don't know always is the same end, we don't know, we are not sure, maybe is just one of the causes, at the end I don't know if it's or not true.

  2. So, would this explain the damage done to cognition from chemotherapy which suppresses immune function?

  3. Anonymous poses an insightful question about chemotherapy. There are several theories about why cognition can be disrupted during chemotherapy but I have not seen any research exploring the ink between suppressed immuno-response and amyloid. However, given that cancer patients tend to regain their previous levels of cognition once chemotherapy is complete, these frequently observed but temporary disruptions are probably not caused by damaging amyloid protein that is ineffectively cleared during therapy.

  4. How different is the new finding, I wonder, from the protein that causes Mad Cow Disease?