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

@article{Macdonald2006PlaquesOA,
  title={Plaques of Alzheimer's disease originate from cysts of Borrelia burgdorferi, the Lyme disease spirochete.},
  author={A. Macdonald},
  journal={Medical hypotheses},
  year={2006},
  volume={67 3},
  pages={
          592-600
        }
}
  • A. Macdonald
  • Published 2006
  • Biology, Medicine
  • Medical hypotheses
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… Expand
Alzheimer's neuroborreliosis with trans-synaptic spread of infection and neurofibrillary tangles derived from intraneuronal spirochetes.
TLDR
It is hypothesize that it is chronic infection of human neurons in Alzheimer's disease that produces neurofibrillary tangles by a pathway similar to the chronic SSPE infection tangle pathway. Expand
Alzheimer's disease - a neurospirochetosis. Analysis of the evidence following Koch's and Hill's criteria
  • J. Miklossy
  • Medicine, Biology
  • Journal of Neuroinflammation
  • 2011
TLDR
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. Expand
Emerging roles of pathogens in Alzheimer disease
  • J. Miklossy
  • Medicine, Biology
  • Expert Reviews in Molecular Medicine
  • 2011
TLDR
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. Expand
Profiling the culprit in Alzheimer's disease (AD): bacterial toxic proteins - Will they be significant for the aetio-pathogenesis of AD and the transmissible spongiform encephalopathies?
TLDR
The profile of bacterial toxic proteins (BTPs) lends support to the hypothesis that BTPs might represent relevant culprits capable to cue and/or promote neuro-degeneration in both AD and the tSEs. Expand
Lyme Disease: Beyond Erythema Migrans
TLDR
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. Expand
Role of Infection in the Pathogenesis of Alzheimer’s Disease
TLDR
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. Expand
Lyme Neuroborreliosis - The Mystifying Pitfall: "Neuropathology and Current Therapeutics".
TLDR
There are very few patents or discoveries made on borrelia infection snatches exact attention towards more focused and targeted research for cure. Expand
Detecting Borrelia Spirochetes: A Case Study With Validation Among Autopsy Specimens
TLDR
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. Expand
Chronic or Late Lyme Neuroborreliosis: Analysis of Evidence Compared to Chronic or Late Neurosyphilis
TLDR
Observations represent evidences that Borrelia burgdorferi in an analogous way to Treponema pallidum is responsible for the chronic/late manifestations of Lyme neuroborreliosis. Expand
Lyme Neuroborreliosis: Mechanisms of B. burgdorferi Infection of the Nervous System
TLDR
The molecular mechanisms of spirochete entry into the brain and the role B. burgdorferi sensu stricto genotypes play in CNS infectivity are explored and understanding infectivity can provide therapeutic targets for LNB treatment and offer public health understanding of the B. burglorferi Sensu stricta genotypes that cause long-lasting symptoms. Expand
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 25 REFERENCES
Beta-amyloid deposition and Alzheimer's type changes induced by Borrelia spirochetes
TLDR
Exposure to Borrelia burgdorferi spirochetes and to the inflammatory bacterial lipopolysaccharide indicates that host responses similar in nature to those observed in AD may be induced by exposure to bacteria or to their toxic products. Expand
Borrelia burgdorferi persists in the brain in chronic lyme neuroborreliosis and may be associated with Alzheimer disease.
TLDR
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. Expand
Alzheimer's disease—a spirochetosis?
TLDR
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. Expand
Borrelia in the brains of patients dying with dementia.
TLDR
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. Expand
Concurrent neocortical borreliosis and Alzheimer's disease.
TLDR
The authors propose that, as occurs in tertiary neurosyphilis and general paresis of the insane, Borrelia species may invade the brain, remain in a latent state for many years, and cause dementia in the absence of other focal neurologic deficits. Expand
P3-197 Cystic borrelia in Alzheimer’s disease and in non-dementia neuroborreliosis
TLDR
While the precise nature of the protein remains elusive, characterization of such familial FTLD-U patients would be helpful in identifying a common denominator in the pathogenesis of familial and the more prevalent sporadic FT LD-U. Expand
The Significance of Measles Virus Antigen and Genome Distribution in the CNS in SSPE for Mechanisms of Viral Spread and Demyelination
TLDR
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. Expand
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 fromExpand
Clonal expansion of hypermutated measles virus in a SSPE brain.
TLDR
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. Expand
Transfection "Junk" DNA - a link to the pathogenesis of Alzheimer's disease?
TLDR
It is hypothesized that spirochetal DNA gains access to the intracellular compartment of nerve cells during the subclinical latency phase of neuroborreliosis and chemically combines with human DNA to offer an important new cognitive model for the detection of occult infections as the root causes for the Tauopathies. Expand
...
1
2
3
...