*Updated 11th Jul 2016
Harvard researchers unveil new Alzheimer’s theory
Dr. Herbert B. Allen and his colleagues at Drexel University, Philadelphia have confirmed the presence of bacterial biofilm substance in autopsy brain tissue from victims of Alzheimer’s disease.
The extracellular polysaccharide matrix of the biofilms was detected using periodic acid Schiff (PAS) stain, and co-localised with the beta-amyloid in the plaques, which are the hallmark of Alzheimer’s.
In summer 2015, in a groundbreaking series of experiments, Dr. Alan MacDonald found Borrelia biofilms in 1000 consecutive Alzheimer’s plaques from a series of five patients’ hippocampal specimens. (The hippocampus, a memory centre , is one of the most catastrophically affected regions of the brain in Alzheimer’s.)
Borrelia miyamotoi is classified as a relapsing-fever type bacteria, but is associated with Lyme disease. Biofilms of this bacteria were identified by Dr. MacDonald using highly specific Molecular Beacon DNA probes for Borrelia which he had recently developed. The biofilms were shown to occupy exactly the same areas as the Beta-amyloid in the plaques with the help of Congo red and/or Thioflavin T stains for amyloid.
The work of Dr. Allen’s team further confirms the many findings by Dr. Alan MacDonald and Dr. Judith Miklossy over the years implicating spirochaetes in Alzheimer’s, a soul-destroying illness afflicting tens of millions worldwide.
The beta-amyloid plaques have long been presumed by the medical establishment to be the cause of the dementia in Alzheimer’s. But the microscope now tells a different story.
A number of scientists are now advancing the theory that the beta-amyloid may actually be an anti-microbial peptide deployed by the body in defense against infection.
For a look at the Spirochetal Alzheimer’s Blog Site containing links to Dr Alan McDonald’s work got to: https://spirodementia.wordpress.com/drexel-university-team-duplicate-dr-alan-macdonalds-findings-of-bacterial-biofilms-in-alzheimers-plaques/
For a set of PDF slides looking at alzheimer plaques & biofilm + various forms of borrelia go to: https://spirodementia.files.wordpress.com/2015/09/living-plaques-in-alzheimers-disease-contain-living-borrelia-biofilm.pdf
The Paul Duray Research Centre is also looking at plaques & biofilm within alzheimer’s brains – take a look at some of the papers & slides on their site:
What’s even more alarming is that borrelia may hide INSIDE nematode worms causing more problems for the brain which could also lead to alzheimers…
Parasitic Nematode Worms containing Borrelia Endosymbionts in Alzheimer’s Disease
In June 2016, Dr. Alan B. MacDonald, president of the Dr. Paul Duray Research Fellowship Endowment and patron of the Spirochaetal Alzheimer’s Association, became the first scientist to demonstrate the presence of parasitic nematode worms containing endosymbiont Borrelia bacteria in autopsy Alzheimer’s brain tissue.
“Nematode worms, (for example C. elegans), manufacture their very own proteins. One example of these is LEA proteins (Late Embryogenesis-Abundant proteins)..
Once inside the human neuron, the worm LEA proteins produce toxic effects, and eventually form Lewy neurites, and in further retrograde migration/passage backwards towards the nucleus of the neuron, eventually reach the soma regions of the human neuron, where they “round up” to form the rounded Lewy bodies. The Lewy bodies are dumped into the brain after the neuron dies.
It is well established that by injection studies of animal brains with huge excesses of healthy labelled alpha-synuclein proteins, that there is a nerve-to-nerve transmission of these proteins throughout neural networks and that synaptic re-uptake of extra-cellular alpha-synuclein is a reality.
The extension of the Lewy body pathobiology ( worms, LEA proteins, Borrelia endosymbionts, dementia, LBD) to Alzheimer’s disease pathobiology is completely logical, given that 30% of Alzheimer’s disease contains a population of Lewy bodies.
I hypothesise that Parkinson’s and its Lewy bodies (worm endosymbiont Borrelia), Multiple System Atrophy, ALS (with its round bodies inside of wounded neurons), Cortico-basal degeneration, Progressive Supranuclear Palsy, and Fronto-Temporal Dementias including Pick’s Disease, as well as all of the less well known neurodegenerative disorders involving round bodies in neurons will show the same pathology.”
For images & more info go to: https://spirodementia.wordpress.com/parasitic-nematode-worms-containing-borrelia-endosymbionts-in-alzheimers-disease/
In the early ’90s, pathologist Alan MacDonald theorized that Alzheimer’s disease may have a bacterial component. Later, Swiss researcher Judith Miklossy made a profound observation when she showed that neurosyphilis (a bacterial disease of the brain) and Alzheimer’s were essentially identical.
Miklossy and her colleagues found two types of spirochetes (long, corkscrew-shaped bacteria) in the brains of more than 90 percent of Alzheimer’s disease patients: Borrelia burgdorferi, which causes Lyme disease; and periodontal pathogens that are a close relative of syphilis. Studies from other researchers have made similar connections between bacteria and dementia.
The findings intrigued Herbert Allen, MD, chairman of Drexel’s Department of Dermatology, who has treated patients with both Lyme disease and syphilis.
In a 2014 study, Allen showed that eczema may be caused by biofilms — multicellular assemblages of bacteria that exude slimy, glue-like substances. Once bacteria metamorphose into a biofilm, antibiotics can no longer treat them. The 2014 study proposed that staphylococcal bacteria that live on the skin produce a biofilm that blocks sweat ducts, activating the immune system, which causes itching and irritation.
Allen’s newest study, published this week in Neuroinfectious Diseases, suggests that spirochetes in the brain could be operating in the same way to cause Alzheimer’s.
Allen and a team of scientists investigated seven post-mortem brains of Alzheimer’s disease patients, comparing them to 10 control samples from people who had died from other causes.
In each of the Alzheimer’s brains, the researchers saw what they believe to be biofilms. The researchers also identified a protein called TLR 2, which plays a key role in activating the body’s innate immune system.
According to Allen’s hypothesis, the spirochetes enter the brain during a dental procedure or after a person contracts Lyme, and then spin out a protective biofilm. The body’s first responders try to clear the infection, but immune cells cannot penetrate the biofilm matrix that encases the organisms. Instead, the immune system ends up destroying the surrounding tissue. This is exactly what happens in cystic fibrosis.
“So it’s neither the infection, nor the biofilm, nor the beta amyloid that causes the disease, but the body’s own immune system,” Allen says.
For more on the article go to: https://newsblog.drexel.edu/2016/02/10/do-infections-cause-alzheimers-disease/
Since Lyme disease is first and foremost a neurological disease that affects the brain and nervous system (although it affects every system of the body), perhaps one of the most important diseases that people with Lyme disease are at an increased risk for is Alzheimer’s dementia. Indeed, research shows that some chronic infections are linked to Alzheimer’s, including spirochetal infections such as Borrelia, one of the primary infections of Lyme disease.
Historic evidence to support a causal relationship between spirochetal infections and Alzheimer’s disease
Front. Aging Neurosci., 16 April 2015
Following previous observations a statistically significant association between various types of spirochetes and Alzheimer’s disease (AD) fulfilled Hill’s criteria in favor of a causal relationship. If spirochetal infections can indeed cause AD, the pathological and biological hallmarks of AD should also occur in syphilitic dementia…Historic observations and illustrations published in the first half of the 20th Century indeed confirm that the pathological hallmarks, which define AD, are also present in syphilitic dementia. ..These historic observations enable us to conclude that chronic spirochetal infections can cause dementia and reproduce the defining hallmarks of AD. They represent further evidence in support a causal relationship between various spirochetal infections and AD.
They also indicate that local invasion of the brain by these helically shaped bacteria reproduce the filamentous pathology characteristic of AD. Chronic infection by spirochetes, and co-infection with other bacteria and viruses should be included in our current view on the etiology of AD. Prompt action is needed as AD might be prevented.
For full report & illustrations head on down to:
The lack of correlation between the incidence of Lyme disease and deaths due to Alzheimer’s disease cannot reflect the lack of involvement of Borrelia burgdorferi in Alzheimer’s dementia
13 August 2014 by Judith Miklossy in the Journal of Alzheimer’s
I am writing this letter in reference to the recent paper by Danton and Catalano . I have read with interest their investigation based on the anticipation that “If the biological agent Borrelia burgdorferi that causes LD (Lyme disease) also causes AD (Alzheimer’s disease), then areas with the highest levels of LD should have significantly higher numbers of deaths due to AD compared to low LD areas.”
For full letter go to: http://www.j-alz.com/node/384
*Updated 14th Jan 2015
A study on the association between infectious burden and Alzheimer’s disease.
BACKGROUND AND PURPOSE:
Previous studies suggested that the overall burden of prior infections contributes to cardiovascular diseases and stroke. In the present study, the association between infectious burden (IB) and Alzheimer’s disease (AD) was examined.
Antibody titers to common infectious pathogens including cytomegalovirus (CMV), herpes simplex virus type 1 (HSV-1), Borrelia burgdorferi, Chlamydophila pneumoniae and Helicobacter pylori were measured by enzyme-linked immunosorbent assay in 128 AD patients and 135 healthy controls. IB was defined as a composite serological measure of exposure to these common pathogens.
Seropositivities toward zero-two, three and four-five of these pathogens were found in 44%, 40% and 16% of healthy controls but in 20%, 44% and 36% of AD patients, respectively. IB, bacterial burden and viral burden were independently associated with AD after adjusting for age, gender, education, APOE genotype and various comorbidities. Mini-Mental State Examination scores were negatively correlated with IB in all cases. Serum beta-amyloid protein (Aβ) levels (i.e. Aβ40, Aβ42 and total Aβ) and inflammatory cytokines (i.e. interferon-γ, tumor necrosis factor α, interleukin-1β and interleukin-6) in individuals exposed to four-five infectious pathogens were significantly higher than those exposed to zero-two or three pathogens.
IB consisting of CMV, HSV-1, B. burgdorferi, C. pneumoniae and H. pylori is associated with AD. This study supports the role of infection/inflammation in the etiopathogenesis of AD.
*Updated 4th June 2014
Lyme Neuroborreliosis and Dementia
J Alzheimers Dis. 2014 Apr 24. [Epub ahead of print]
Blanc F1, Philippi N1, Cretin B1, Kleitz C2, Berly L2, Jung B1, Kremer S3, Namer IJ4, Sellal F5, Jaulhac B6, de Seze J7.
Objective: To describe patients with dementia and a positive “intrathecal anti-Borrelia antibody index” (AI), specific for neuroborreliosis.
Methods: Among 1,594 patients seen for dementia, we prospectively identified and studied 20 patients (1.25%) with dementia and a positive AI. Patients underwent a battery of neuropsychological tests brain, MRI, FDG-PET, and cerebrospinal fluid (CSF) analysis. An etiological diagnosis of the dementia was made at the end of the follow-up of 5.0 ± 2.9 years.
Results: We found two groups of patients with dementia, the first (n = 7, 0.44%) with certain neuroborreliosis and stability or mild improvement of dementia after treatment by antibiotics and the second (n = 13, 0.81%) with progressive worsening of dementia, despite the antibiotics. In the second group, the final diagnoses were Alzheimer’s disease (AD) (n = 4), AD and Lewy body disease (LBD) (n = 3), LBD (n = 1), FTLD (n = 3), hippocampal sclerosis (n = 1), and vascular dementia (n = 1). We did not observe any differences in cognitive test between the two patient groups at baseline. Brain MRI showed more focal atrophy and FDG-PET showed more frontal hypometabolism in the second group. Tau, p-tau, and Aβ42 concentrations in the CSF were normal in the neuroborreliosis group, and coherent with diagnosis in the second. Conclusion: Pure Lyme dementia exists and has a good outcome after antibiotics.
It is advisable to do Lyme serology in demented patients, and if serology is positive, to do CSF analysis with AI. Neurodegenerative dementia associated with positive AI also exists, which may have been revealed by the involvement of Borrelia in the CNS.
Borrelia burgdorferi persists in the brain in chronic lyme neuroborreliosis and may be associated with Alzheimer disease
Journal of Alzheimer’s Disease 6 (2004) 639–649 639 IOS Press
Judith Miklossya,b,∗, Kamel Khalilib, Lise Gernc, Rebecca L. Ericsond, Pushpa Darekara, Lorie Bollee,
Jean Hurlimanna and Bruce J. Pasterd
Judith Mikklossy is a director of the Prevention of ALZHEIMER’S Foundation: http://www.miklossy.ch/473.html
Plaques of Alzheimer’s disease originate from cysts of Borrelia burgdorferi, the Lyme disease spirochete
Elsevier Press 2006
Alan B. MacDonald *
Dr Alan MacDonald, Pathologist has a an alzheimer borreliosis web page with articles, presentations & videos at: http://alzheimerborreliosis.net/
You can see him speak here at:
Dr MacDonald is also involved in the newly developed Spirochaetal Alzheimer’s Association – their inaugural meeting was held in London UK, on June 4th 2014.. http://www.spirochaetalalzheimersassociation.org/
Stroke, Meningitis, Alzheimer’s Caused by Lyme Disease
Added by Lindsey Alexander on April 5, 2014.
See link below for the full article..
Alan MacDonald, M.D., is a pathologist affiliated with St. Catherine of Siena Medical Center in Smithtown, New York. His current research is concentrated on developing what he refers to as a new biology for Lyme disease, including the use of special DNA probes to detect Borrelia DNA in spinal fluid and in tissue sections from Alzheimer autopsy tissues.
Through his research, and with the help of other leading researchers in the field of molecular and cellular biology, Dr. MacDonald is pioneering a broader understanding about the behavior of Borrelia burgdorferi, the bacteria that causes Lyme disease. He has appeared as an invited lecturer at Lyme symposia, including the ILADS National Scientific Meetings and Columbia University/Lyme Disease Association conferences in Philadelphia, PA, where he presents the findings from his explorations into the connection between Borrelia spirochetal infection and Alzheimer’s disease.
For on interview with Dr MacDonald refer to the link below:
Emerging Role of Infection in Alzheimer’s Disease & Stroke
Treponema pallidum and Borrelia burgdorferi spirochetes, in late syphilis and late Lyme disease can cause cerebral infarct and cognitive decline (dementia) in parenchymatous neurosyphilis and Lyme neuroborreliosis.
The cognitive decline (dementia) is caused by the direct invasion of brain parenchyma by spirochetes (direct parenchymal involvement) years or decades follwoing the primary infection.
Cerebral infarcts in the meningovascular form of neurospirochetoses (Meningovascular form of neurosyphilis and Lyme neuroborreliosis) is not caused by spirochetal invasion of brain tissue. The parenchymal involvement is secondary to the occlusion of the affected meningeal arteries. It may lead to”vascular” dementia.
Consequently, to exclude infection, e.g. Borrelia infection in patients with stroke, particularly in endemic areas of Lyme disease is primordial.
Here we describe the line of research we have followed during the last 15 years with respect to the involvement of spirochetes in Alzheimer’s disease and in cerebral infarcts. This line of research represents series of experiments, listed below, which are linked to each other. The goal was to answer the question, whether several types of spirochetes, including Borrelia burgdorferi, may be involved in Alzheimer disease and in stroke.
1. ALZHEIMER DISEASE
2. CHRONIC INFLAMMATION AND ALZHEIMER’S DISEASE
3. BACTERIA, INCLUDING SPIROCHETES ARE POWERFUL STIMULATORS OF INFLAMMATION AND ARE AMYLOIDOGENIC
4. CHRONIC BACTERIAL INFECTION CAN CAUSE DEMENTIA
6. OUR CONTRIBUTION TO THIS EMERGING FIELD OF RESEARCH
8. PUBLICATIONS FROM OUR LABORATORY RELATED TO THE INVOLVEMENT OF SPIROCHETES IN STROKE (CEREBROVASCULAR INFARCT) AND ALZHIEMER’S DISEASE
Alzheimer’s disease – a neurospirochetosis. Analysis of the evidence following Koch’s and Hill’s criteria