Plaques of Alzheimer’s disease originate from cysts of Borrelia burgdorferi, the Lyme disease spirochete
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)
- et al.
Concurrent neocortical Borreliosis and Alzheimer’s disease
Hum Pathol
(1987) Transfection “Junk” DNA – A link to the pathogenesis of Alzheimer’s disease?
Med Hypotheses
(2006)- et al.
Beta amyloid deposition and Alzheimer’s type changes induced by Borrelia Spirochetes
Neurobiol Aging
(2006) Concurrent neocortical Borreliosis and Alzheimer’s disease – demonstration of a spirochetal cyst form
Ann N Y Acad Sci
(1988)
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