Lyme and Alzheimer's

The words cromolyn, microglia, beta amyloid protein, Alzheimer’s disease, pathogens and Lyme came together, today, at Harvard, where I am attending a continuing education meeting. Dr. Tanzi, a neuroscientist and star Harvard Alzheimer’s researcher spoke of the connection between Alzheimer’s disease and brain pathogens.  Dr. Tanzi, author and researcher, discovered Alzheimer’s genes, wrote seminal papers about Alzheimer’s and he hosts TV shows on PBS. Yet, recent research papers, were rejected by the editors/peer reviewers of major journals, because, “they have a different philosophy.”  He talked about changing paradigms and it sounded familiar. I wanted to say: publishable findings, in vitro and in vivo results are facts – science. Philosophy is neither. “Philosophy” has historically stood in the way of medical and scientific advancement. (Or do we live in a world of “alternative facts).  The Lyme—Alzheimer’s connection has been discussed by neurobiology researcher Ruth Itzhaki in Scientific American and this year Psychology Today warned us of the coming epidemic of Lyme dementia. The related work of Miklossy and Alan MacDonald is ongoing and well known to many. 

It is well known that Alzheimer’s is related to beta amyloid plaque and associated tangles. It is also well known that the brain is far from the sterile domain we once thought it was.  A zoo of microbes, replete with biofilms inhabits our brains. Some of the unwanted occupants are, HHV6, Chlamydia pneumonia, spirochetes (Lyme and others), other bacteria, fungal pathogens, toxoplasmosis and other protozoans.  

The brain’s immune system may be provoked by one of these germs triggering an inflammatory cascade. Glial cells, the resident immune cells in the brain activate and stimulate amyloid, a natural response to infection, like other well-known endogenous antimicrobial peptides.  If the reaction is overheated, excessive amyloid accumulates forming plaques. The B amyloid response is a natural, and generally a beneficial response.  Some amyloid is good, too much is bad and none is also bad.  Vaccine trials directed against amyloid have failed, perhaps for this reason.  Humans are genetically diverse. Some of us tolerate amyloid plaques and for some of us they are disastrous. 

Harvard researchers screened drug libraries looking for microglial--amyloid “goldilocks” drugs. The most promising is cromolyn (very early stages of investigation), an asthma drug, When researchers screen drug libraries they frequently surprising, inexpiable results. It is fortuitous when FDA approved drugs can be repurposed.  Cromolyn is a well-known mast cell stabilizer. Perhaps the dance between glial cells and mast cells in neuroinflammation is relevant. Perhaps not. 

This is important research to keep pace with (although it can be hard to find studies which go unpublished).

Dr. Tanzi said today we wait to treat Alzheimer's until patients are symptomatic (with ineffective drugs), by then the brain is already full of plaques and tangles. It like closing the proverbial barn door when the horse is already out in the fields. 

Imagine if we didn't worry about heart disease until someone keels over with chest pain, only then considering the person's blood pressure and cholesterol. 

We need early intervention but we must have a much better understanding of the disease.  The use of antibiotics may be inevitable, unless they come up with something better.