A new study by Harvard researchers lends further weight to the possibility that an infection with spirochaete bacteria underlies Alzheimer’s disease.
Professor Rudolph Tanzi and his colleague Dr. Robert Moir have found that beta-amyloid, a protein traditionally seen as the “villain” in Alzheimer’s, actually protected cultured human nerve cells from infection in vitro.
Beta-amyloid, found in the brain plaques that are a hallmark of Alzheimer’s, has long been viewed as the culprit responsible for the wholesale destruction of brain tissue that occurs in dementia.
Yet despite billions invested in development of anti-amyloid therapies, no drug to date has proven to cure or even slow the relentless march of the disease. The Harvard researchers believe that the amyloid-as-cause theory is too simplistic, and that the beta-amyloid could actually be an anti-microbial peptide produced by the body’s innate immune system in defence.
Tanzi and Moir also experimented with mice and tiny roundworms, which they genetically engineered to express human beta-amyloid. They found the animals were protected from infection with salmonella and candida.
Anti-microbial peptides (AMPs) are believed to be an ancient protective mechanism found across the animal kingdom, playing a vital role in the immune system’s first line of defense against pathogens.
Cells of the innate immune system release AMPs known as cathelicidins, destroying invaders. They are also produced by skin cells in response to infection or injury.
Parallels between the human cathelicidin, “LL37”, and beta-amyloid were the inspiration for Moir and Tanzi’s current line of research.
In 2015, our patron Alan MacDonald, MD, FCAP, director of the Paul Duray Research Fellowship Endowment Inc., detected Borrelia bacteria in 1000 consecutive amyloid brain plaques from five victims of Alzheimer’s.
Borrelia, the bacteria responsible for Lyme disease and relapsing fever, were detected using Fluorescent in situ Hybridisation (FISH) with Molecular Beacon DNA probes. These probes are highly specific for their target DNA, only fluorescing when there is a 100% match.
Up till recently, it had been thought that Alzheimer plaques were simply composed of beta-amyloid – but Dr. MacDonald found in the five cases he examined that virtually the entire substance of the plaque was positive for Borrelia DNA, coated with beta-amyloid.
These specific DNA probes have detected Borrelia in living and deceased patients, who had been told they could not have a Borrelia infection due to negative results on standard antibody-based tests for Lyme disease. These antibody tests are still recommended by the Centers for Disease Control (CDC), and are still used routinely throughout the world, despite their proven insensitivity.
The detection of Borrelia, in biofilm form, filling Alzheimer’s plaques while absent from the surrounding healthy brain tissue is evidence that warrants attention from the scientific community. Indeed, the presence of bacterial biofilms (not identified to species level) in Alzheimer plaques has now been confirmed by a team at Drexel University.
Bacterial biofilms (see image below) are highly-organised, kill-resistant, multi-cellular communities of microbes.
While Prof. Tanzi has suggested that the AMP may be triggered by an infection, or simply the immune system’s “perception” of infection, Dr. MacDonald’s findings suggest the infection is not only real, but very much ongoing. Biofilms always signify chronic infection.
Presentation by Alan MacDonald MD FCAP on borrelia biofilm in Alzheimer plaques: