More about Alzheimer's disease as an autoimmune disease

We wrote recently about new thinking with regard to what causes Alzheimer's disease to begin and to progress.  The post was based on the work of one team from Washington University, St. Louis, but they are not alone.  My friend Teale recently shared with me a story from ScienceAlert.com written by a researcher from the Krembil Brain Institute, part of the University Health Network in Toronto.  Their new hypothesis was published here in Alzheimer's and Dementia; the journal of the Alzheimer's Association. 

Their research suggests there is a similarity between certain fat molecules in brain cells and fat molecules in some bacteria.  Instead of attacking the bacteria, the brain's unique immune system confuses the molecules and attacks neurons, not bacteria.  This may spark the activation and dormancy cycle we discussed in the previous post.  And consistent with what we said in Beating the Dementia Monster, these researchers propose that beta amyloid is actually a normal product of the immune system, and its function is to protect the neurons.  So getting rid of beta amyloid may be a bad strategy.  This, of course, challenges the idea that we can fight Alzheimer's disease by removing amyloid plaques, the principle behind why Aduhelm and Leqembi should work. 

I would speculate that this abnormal immune response may be encouraged by conditions in the brain, such as susceptibility to inflammation and oxidation.  These, in turn, are influenced by genetic makeup, diet, exercise, and other lifestyle characteristics.  And where brain cells have been attacked by the autoimmune response, the generation of BDNF during exercise and intermittent fasting strengthens and replenishes them.

As we've said before, what this really tells us is that Alzheimer's is an incredibly complex disease.  We just don't understand it very well at all.