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

  title={Plaques of Alzheimer's disease originate from cysts of Borrelia burgdorferi, the Lyme disease spirochete.},
  author={Alan B. Macdonald},
  journal={Medical hypotheses},
  volume={67 3},

Alzheimer's disease - a neurospirochetosis. Analysis of the evidence following Koch's and Hill's criteria

  • J. Miklossy
  • Medicine, Biology
    Journal of Neuroinflammation
  • 2011
A probable causal relationship between neurospirochetosis and AD is shown and adequate antibiotic and anti-inflammatory therapies are available, as in syphilis, one might prevent and eradicate dementia.

Emerging roles of pathogens in Alzheimer disease

  • J. Miklossy
  • Biology
    Expert Reviews in Molecular Medicine
  • 2011
Aβ has been shown to be a pore-forming antimicrobial peptide, indicating that Aβ accumulation might be a response to infection, and dementia might be prevented by combined antibiotic, antiviral and anti-inflammatory therapy.

Borrelia burgdorferi Co-Localizing with Amyloid Markers in Alzheimer’s Disease Brain Tissues

Evidence is provided for a likely association between B. burgdorferi infections and biofilm formation, AD pathology, and chronic neurodegenerative diseases.

Lyme Disease: Beyond Erythema Migrans

The very presence of the organisms in the brains following supposedly effective treatment for Lyme disease is contradictory and should be the starting point for diagnosis and treatment.

Role of Infection in the Pathogenesis of Alzheimer’s Disease

This work has shown that peripheral infections may have a role to play in accelerating neurodegeneration in Alzheimer’s disease by activating already primed microglial cells within the CNS.

Lyme Neuroborreliosis - The Mystifying Pitfall: "Neuropathology and Current Therapeutics".

There are very few patents or discoveries made on borrelia infection snatches exact attention towards more focused and targeted research for cure.

Detecting Borrelia Spirochetes: A Case Study With Validation Among Autopsy Specimens

Methods to reliably detect Borrelia burgdorferi, the spirochete bacteria responsible for Lyme disease, in autopsy specimens of patients with a history of neurocognitive disease offer proof of the principle that persistent infection with the Lyme disease spiroChete may have lingering consequences on the CNS.

A Novel Approach to the Treatment and Prevention of Alzheimer’s Disease Based on the Pathology and Microbiology

  • H. Allen
  • Biology, Medicine
    Journal of Alzheimer's disease : JAD
  • 2021
It is very likely possible that AD could be prevented by periodic administration of penicillin (PCN), which would kill the spirochetes before they made biofilms, and it may be possible to slow or prevent further decline in early AD by administration of PCN together with a biofilm disperser.



Beta-amyloid deposition and Alzheimer's type changes induced by Borrelia spirochetes

Borrelia burgdorferi persists in the brain in chronic lyme neuroborreliosis and may be associated with Alzheimer disease.

The data indicate that Borrelia burgdorferi may persist in the brain and be associated with amyloid plaques in AD, and suggest that these spirochetes, perhaps in an analogous fashion to Treponema pallidum, may contribute to dementia, cortical atrophy and amyloids deposition.

Alzheimer's disease—a spirochetosis?

Observations that in 14 autopsy cases with histopathologically confirmed AD, spirochetes were found in blood and cerebrospinal fluid and, moreover, could be isolated from brain tissue suggest that spiroChetes may be one of the causes of AD and that they may be the source of the β amyloid deposited in the AD brain.

Borrelia in the brains of patients dying with dementia.

Indirect immunofluorescence, using monoclonal antibodies specific for Borrelia species, resulted in fluorescence of spirochetes that had previously been identified by darkfield microscope examination of autopsy brain tissues from two patients with dementia.

The Significance of Measles Virus Antigen and Genome Distribution in the CNS in SSPE for Mechanisms of Viral Spread and Demyelination

The relationship between myelin destruction and oligodendrocytic infection suggested that the demyelination may be solely the result of virus infection, and findings may suggest viral spread in a cephalo-caudal direction, probably by transneuronal spread.

Rabies: interactions between neurons and viruses. A review of the history of Negri inclusion bodies

The first clear-cut description of a virus-nerve cell interaction was made by Adelchi Negri in 1903 with the detection of cytoplasmic bodies (Negri bodies) in subsets of neurons in the brain from

Clonal expansion of hypermutated measles virus in a SSPE brain.

Despite the presence of MV variants with genes encoding the intact matrix protein open reading frame, M protein could not be detected in any of the brain regions.

Transfection "Junk" DNA - a link to the pathogenesis of Alzheimer's disease?