Second Provocative Fact:
In 1982 when the cause of Lyme disease was found to be a spirochete, immediately the CDC tried to distance this Lyme disease from a group of diseases caused by Borrelia spirochetes known as Tick Borne Relapsing Fevers. We can no longer do this since the Relapsing Fever Borrelia miyamotoi was discovered to be in the same hard-shelled Ixodes ticks as the Lyme bacteria.
- miyamotoi causes a Lyme-like disease in humans. B. miyamotoi likes warmer temperatures than B. burgdorferi, and B. miyamotoi enters the brain and can form biofilms in amyloid plaques just like B. burgdorferi.
What we discovered in 2015 was even more disturbing.
Borrelia miyamotoi a Relapsing Fever borrelia, was routinely being seen inside human brains. As Alan continued to do his brain autopsy research on Alzheimer’s brains from Harvard Brain Bank, he found, using fluorescent FISH stains, that B. miyamotoi was not only in many of the brain tissue samples, but that it was usually associated with amyloid plaques.
It may turn out that B. miyamotoi is as prevalent as, or even predominant over B. burgdorferi in human brains and dementia patients.
This was bad news because B. miyamotoi is not detected with the Lyme serology tests that are used, and doctors rarely think to test for any Relapsing Fever Borrelia. So this kind of brain infection probably goes undiagnosed for decades. Despite the severe neurologic symptoms, the patient exhibits, the patients most often are left untreated leading to dementia.
Above: The same Alzheimer plaque is imaged twice – first, after staining for the presence of beta-amyloid, then, after FISH staining for DNA of Borrelia.
The correlation with amyloid plaques was intriguing.
Looking at research done by others, it was obvious that Borrelia had a profound effect on the brain cells.
Jorge Benach showed that when Borrelia was added to rat-brain culture, the brain cells would immediately swell and die. Jill Livengood and Robert Gilmore of CDC showed the Borrelia burgdorferi has a tendency to seek out blood vessel lining cells, brain glial cells (cells which function in support of the nerve cells), and brain neurons.
When Judith Miklossy isolated Borrelia bacteria from a human brain with dementia, she cultured the cells along with rat-brain cells that were also grown in culture. The brain cells enhanced with added microglia, started to overproduce amyloid-precursor-protein (APP). This APP quickly converted to beta-sheet amyloid, the hallmark of Alzheimer’s. Then other markers of Alzheimer’s also occurred: hyper phosphorylation of microtubule protein tau, neurofibrillary tangles, and vacuolization. In short Borrelia induced amyloid formation and became toxic to brain cells.
What we showed was that every amyloid plaque we stained for Borrelia had associated with it a biofilm of either B. burgdorferi or B. miyamotoi. What for centuries had been seen with silver-stain as amorphous globs, now shone brightly as Borrelia spirochetes.
Many people in the Lyme community suspected that Lyme disease was somehow associated with dementia, but the Lyme tests kept coming back negative. We now had the answer: Borrelia miyamotoi was a common pathogen of the brain hidden away from the immune system behind the blood-brain-barrier and sequestered inside biofilms and brain cells.
Of course the Lyme tests were negative!
Now the question was: What about other Neurologic diseases like Parkinson’s, Multiple Sclerosis and Lewy-Body dementia?
What this means to patients:
The presence of Borrelia in Alzheimer’s plaques means some dementia patients if caught early, may improve on antibiotics or stop the progression of the disease. But Lyme tests will not detect B. miyamotoi so treatment must be done by clinical diagnosis and response to therapy. It is likely that lengthy therapy is needed, perhaps life-long treatment. (Later we will see why adding an antiparasite medicine like albendazole might be the first step.)