Plaques of Alzheimer’s disease originate from cysts of Borrelia burgdorferi, the Lyme disease spirochete

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Summary

Here is hypothesized a truly revolutionary notion that rounded cystic forms of Borrelia burgdorferi are the root cause of the rounded structures called plaques in the Alzheimer brain. Rounded “plaques’ in high density in brain tissue are emblematic of Alzheimer’s disease (AD). Plaques may be conceptualized as rounded “pock mark-like” areas of brain tissue injury. In this century, in brain tissue of AD, plaques are Amyloid Plaques according to the most up to date textbooks. In the last century, however, Dr. Alois Alzheimer did not require amyloid as the pathogenesis for either the disease or for the origin of its plaques. Surely, amyloid is an event in AD, but it may not be the primal cause of AD. Indeed in plaques, amyloid is regularly represented by the “congophilic core” structure which is so named because the waxy amyloid material binds the congo red stain and is congophilic. However an accepted subset of plaques in AD is devoid of a congophilic amyloid core region (these plaques “cotton wool” type plaques, lack a central congophilic core structure). Furthermore, there is “plaque diversity” in Alzheimer’s; small, medium and large plaques parallel variable cystic diameters for Borrelia burgdorferi. Perturbations of AD plaque structure (i.e. young plaques devoid of a central core and older plaques with or without a central core structure) offer room for an alternate pathway for explanation of ontogeny of the plaque structures. If amyloid is not required to initiate all of the possible plaques in Alzheimer’s, is it possible that amyloid just a by product of a more fundamental primal path to dementia? If a byproduct status is assigned to amyloid in the realm of plaque formation, then is amyloid also an epiphenomenon rather than a primary pathogenesis for Alzheimer’s disease. In the “anatomy is destiny” model, cysts of borrelia are always round. Why then not accept roundness as a fundamental “structure determines function” argument for the answer to the mystery of why Alzheimer plaques are always round? Parataxis causality, a concept borrowed from philosophy, is the error that comes from linking two events, which occur contemporaneously or in close proximity to one another with a cause and effect relationship. Parataxis tells us that what appears to be cause and effect in the couplet “amyloid plaque” merely by a proximity relationship may be “spurious causality” which is a cognitive dead end.

Introduction

The first published report of a cystic form for Borrelia burgdorferi, the etiologic agent of Lyme Borreliosis, was offered as a video poster presentation “Concurrent Neocortical Borreliosis and Alzheimer’s Disease – Demonstration of s Spirochetal Cyst Form”, at the International Conference on Lyme Disease and Related Disorders which was sponsored by the New York Academy of Sciences and the New York Department of Health on September 14–16, 1987 [1].

Subsequently, beginning in 1994, published reports of cysts of Borrelia burgdorferi began to appear in the peer reviewed literature, and to date more than 40 articles from workers in Europe and the United States have ratified the scientific validity of rounded cystic forms of the spirochete emerging from the corkscrew forms under conditions of adversity (starvation, osmolar shock, acid pH, and antibiotic effects) [2].

Alzheimer’s disease associated with corkscrew shaped Borrelia spirochetes in autopsy brain tissue has been reported by two pathologists [3], [4], [5], [6], but cystic forms of Borrelia burgdorferi in Alzheimer brain tissues have only been the focus of research for one pathologist in the world [7].

Cystic profiles of borrelia closely correspond to the diverse profiles of plaques, namely they are always round, and are capable of increase in size from little to big as cystic spirochetal growth progresses. Maturation of cysts parallels “maturation” of plaques of increasing age, based on observations of spirochetal cysts in a tissue culture model. Cystic spirochetes in tissue culture incorporate injured cells into their interior regions. Amyloid fibrils within blood vessels of the brain may wind up within the plaque region, now redefined as spirochetal cyst “territory”, merely because the rounded cyst “landed on a blood vessel” which contained amyloid in its wall. DNA hybridization methods demonstrate the areas where Borrelia DNA is deposited in the Alzheimer brain. Hybridizations using DNA from the spirochete develop a “map” of the terrain of the brain where, like little rounded villages and cities, rounded “map sites” of spirochetal DNA appear. Spirochetal sites on these “DNA maps” match the sites of the plaques in the Alzheimer brain. Now is the time for a new opportunity to re-evaluate Alzheimer’s disease with DNA mapping methods.

Section snippets

The hypothesis

Cystic spirochetes show close structural similarities to the profiles of AD plaques. First, will be images of the plaques, second will be spirochetal cysts.

Therefore, the hypothesis was formulated that the cysts of the spirochete are the actual cause of the plaques.

Currently, there is no iterated model to explain, in the absence of the cystic pathway to plaque formation in AD, a mechanism to define the facts that plaques in AD are virtually always round in contour, variable in diameter and

Evaluation of the hypothesis

Molecular interrogation of Alzheimer brain tissues has yielded evidence of specific flagellin B sequences which are recoverable from DNA digests of autopsy frozen brain tissues provided by the Harvard University McLean Hospital Brain Bank, with seven cases yielding essentially identical and heretofore unique PCR products which have been reported previously [8].

The specific DNA of Borrelia burgdorferi which was recovered from the Harvard Alzheimer brains was used to design DNA probes (molecular

Empiric data

In vitro Culture of Cysts of Borrelia burgdorferi from the spinal fluid of another patient (no dementia). Spinal fluid negative for spirochetes by darkfield at commencement of culture, with cysts detected at 16 months later. Spinal fluid antibodies positive in ImmunoBlot at a regional reference laboratory.

Line drawings of the interconversions of corkscrew shaped Borrelia burgdorferi into Cystic spirochetes.

Line drawings of the interconversion of corkscrew shaped Borrelia burgdorferi into

Consequences of the hypothesis

The hypothetical proof that ALL of the plaques in the brains of patients with Alzheimer’s disease are positive for the DNA of Borrelia burgdorferi would silence the argument, now currently discussed by some neuropathologists which is as follows: “… coincidence links those cases of Alzheimer’s disease showing detection of antibodies in blood testing against Borrelia burgdorferi…” This argument is wrapped in the caveats that Alzheimer’s is a relatively common disease. Lyme borreliosis is a common

Acknowledgements

This work was supported by a research grant from the Turn the Corner Foundation, New York and ILADS (International Lyme Disease and Related Disorders Society), and generous institutional support from the St. Catherine of Siena Medical Center, Smithtown, New York.

The Harvard University McLean Hospital Brain Bank provided frozen Alzheimer’s disease brain tissues for the molecular interrogation studies by polymerase chain reaction with flagellin B primer oligonucleotides.

Sequencing of PCR products

References (9)

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