Researchers Identify Virus and Two Types of Bacteria as Major Causes of Alzheimer’s

Image shows an old lady looking out of a window.
This major call for action is based on substantial published evidence into Alzheimer's. Image is adapted from the University of Manchester press release.

A worldwide team of senior scientists and clinicians have come together to produce an editorial which indicates that certain microbes – a specific virus and two specific types of bacteria – are major causes of Alzheimer’s Disease. Their paper, which has been published online in the highly regarded peer-reviewed journal, Journal of Alzheimer’s Disease, stresses the urgent need for further research – and more importantly, for clinical trials of anti-microbial and related agents to treat the disease.

This major call for action is based on substantial published evidence into Alzheimer’s. The team’s landmark editorial summarises the abundant data implicating these microbes, but until now this work has been largely ignored or dismissed as controversial – despite the absence of evidence to the contrary. Therefore, proposals for the funding of clinical trials have been refused, despite the fact that over 400 unsuccessful clinical trials for Alzheimer’s based on other concepts were carried out over a recent 10-year period.

Opposition to the microbial concepts resembles the fierce resistance to studies some years ago which showed that viruses cause certain types of cancer, and that a bacterium causes stomach ulcers. Those concepts were ultimately proved valid, leading to successful clinical trials and the subsequent development of appropriate treatments.

Professor Douglas Kell of The University of Manchester’s School of Chemistry and Manchester Institute of Biotechnology is one of the editorial’s authors. He says that supposedly sterile red blood cells were seen to contain dormant microbes, which also has implications for blood transfusions.

“We are saying there is incontrovertible evidence that Alzheimer’s Disease has a dormant microbial component, and that this can be woken up by iron dysregulation. Removing this iron will slow down or prevent cognitive degeneration – we can’t keep ignoring all of the evidence,” Professor Douglas Kell said.

Professor Resia Pretorius of the University of Pretoria, who worked with Douglas Kell on the editorial, said “The microbial presence in blood may also play a fundamental role as causative agent of systemic inflammation, which is a characteristic of Alzheimer’s disease – particularly, the bacterial cell wall component and endotoxin, lipopolysaccharide. Furthermore, there is ample evidence that this can cause neuroinflammation and amyloid-β plaque formation.”

The findings of this editorial could also have implications for the future treatment of Parkinson’s Disease, and other progressive neurological conditions.

About this Alzheimer’s disease research

Source: University of Manchester
Image Credit: The image is adapted from the University of Manchester press release.
Original Research: Full open access editorial for “Microbes and Alzheimer’s Disease” by Itzhaki, Ruth F.; Lathe, Richard; Balin, Brian J.; Ball, Melvyn J.; Bearer, Elaine L.; Bullido, Maria J.; Carter, Chris; Clerici, Mario; Cosby, S. Louise; Field, Hugh; Fulop, Tamas; Grassi, Claudio; Griffin, W. Sue T.; Haas, Jürgen; Hudson, Alan P.; Kamer, Angela R.; Kell, Douglas B.; Licastro, Federico; Letenneur, Luc; Lövheim, Hugo; Mancuso, Roberta; Miklossy, Judith; Lagunas, Carola Otth; Palamara, Anna Teresa; Perry, George; Preston, Christopher; Pretorius, Etheresia; Strandberg, Timo; Tabet, Naji; Taylor-Robinson, Simon D.; and Whittum-Hudson, Judith A. in Journal of Alzheimer’s Disease. Published online March 8 2016 doi:10.3233/JAD-160152


Microbes and Alzheimer’s Disease

We are researchers and clinicians working on Alzheimer’s disease (AD) or related topics, and we write to express our concern that one particular aspect of the disease has been neglected, even though treatment based on it might slow or arrest AD progression. We refer to the many studies, mainly on humans, implicating specific microbes in the elderly brain, notably herpes simplex virus type 1 (HSV1), Chlamydia pneumoniae, and several types of spirochaete, in the etiology of AD. Fungal infection of AD brain [5, 6] has also been described, as well as abnormal microbiota in AD patient blood. The first observations of HSV1 in AD brain were reported almost three decades ago]. The ever-increasing number of these studies (now about 100 on HSV1 alone) warrants re-evaluation of the infection and AD concept.

AD is associated with neuronal loss and progressive synaptic dysfunction, accompanied by the deposition of amyloid-β (Aβ) peptide, a cleavage product of the amyloid-β protein precursor (AβPP), and abnormal forms of tau protein, markers that have been used as diagnostic criteria for the disease. These constitute the hallmarks of AD, but whether they are causes of AD or consequences is unknown. We suggest that these are indicators of an infectious etiology. In the case of AD, it is often not realized that microbes can cause chronic as well as acute diseases; that some microbes can remain latent in the body with the potential for reactivation, the effects of which might occur years after initial infection; and that people can be infected but not necessarily affected, such that ‘controls’, even if infected, are asymptomatic

“Microbes and Alzheimer’s Disease” by Itzhaki, Ruth F.; Lathe, Richard; Balin, Brian J.; Ball, Melvyn J.; Bearer, Elaine L.; Bullido, Maria J.; Carter, Chris; Clerici, Mario; Cosby, S. Louise; Field, Hugh; Fulop, Tamas; Grassi, Claudio; Griffin, W. Sue T.; Haas, Jürgen; Hudson, Alan P.; Kamer, Angela R.; Kell, Douglas B.; Licastro, Federico; Letenneur, Luc; Lövheim, Hugo; Mancuso, Roberta; Miklossy, Judith; Lagunas, Carola Otth; Palamara, Anna Teresa; Perry, George; Preston, Christopher; Pretorius, Etheresia; Strandberg, Timo; Tabet, Naji; Taylor-Robinson, Simon D.; and Whittum-Hudson, Judith A. in Journal of Alzheimer’s Disease. Published online March 8 2016 doi:10.3233/JAD-160152

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  1. There is a similarity in the symptoms among Dementia, Autism, ME/CFS/FM, Lyme disease, GWI, ALS, MCTD, SLE, RA, Multiple sclerosis, Malignancy (Cancer) and Mycoplasma Infectious Diseases (MID).

    There might have been misunderstood, misdiagnosed, mistreated or over looked. For this, it had been important to establish reliable diagnostics.

    Current Mycoplasma diagnostic tests are not able to differentiate between asymptomatic carriage and symptomatic infection.

    PCR method is problematic especially for chronic systemic infectious diseases. One major reason for these misunderstanding comes from the problem of PCR method, because it is very difficult to detect mycoplasma by PCR constantly. “It is negative” does not mean “there is not mycoplasma”. It crucially depend on how they take samples, where to take sample, and how to store the samples. There are also problems to see clinically.

    Fortunately, the cutting-edge technology based on the mycoplasma species-specific glycolipid-antigens, has made it possible to measure the amount of specific antibodies.

    Recently, this paper has published, and this might help doctors understand/aware the concept of this medicine.

    A novel therapeutic strategy for mycoplasma infectious diseases
    Kazuhiro Matsuda, Personalized Medicine Universe 2015 4:32-39

    The new technology provides a reliable marker to follow the state of Mycoplasma Infectious Diseases (MID) by monitoring antibody titer fluctuations from baseline. It therefore becomes possible to follow individual patients.

  2. this makes total and complete sense to me. i immediately connected it to the chickenpox/shingles correlation. the possible causes of AD listed in this article are definitely appropriate to my husband. my husband was diagnosed with age related dementia/AD in june 2012 by mri (at age 80, when he was still actively pastoring a church). he had had several mri over a period of years showing progressive plaque build up with some symptomatology. after major open heart surgery in may 2013 there was a major change in his status mentally for the worse and with a slow downhill slide, along with physical weakening, such as in his balance & hearing, even tho he now exercised on a regular basis – something he had not done in more than 30 years. as of january 2016, he is now on dialysis, with another drop in mental status. he lost a sister diagnosed with AD in april 2015 at the age of 95 and has a sister with mild dementia who just reached the age of 99. we did almost not accept going on the dialysis due to the AD, even knowing it would have meant imminent death. living with this disease on a daily basis, the current ‘meds’ for it are worse than the disease itself, are too expensive, & many times of no use. we need to find a way to stop this disease. these clinical trials must be funded. the treatments are there for us to find & are probably already on our shelves now.

  3. In the editorial of the Journal of Alzheimer Disease , published in 8 March 2016 with the title “MICROBES AND ALZHEIMER’S DISEASE”,the dozens of prestigeous researchers of prestigeous universtities of dozens of countries around the world that wrote the milestone text of it very interesting editorial , agree that herpes simplex virus type 1 , Chlamydia pneumoniae, and several types of spirochaete (as Borrelia of Lyme disease) , fungal infections,etc. can be related as some triggers (but NOT as causes) of Alzheimer disease.Extra Virgin Coconut Oil is empirically used as mitochondrial function improver and as alternative fuel to the brain in AD and others dementias , still without scientific foundation, but with hundreds of empirical testimonies by patients , caregivers and relatives of patients that gives some improve in dementias as AD.SUGGESTION FOR RESEARCH:EXTRA VIRGIN COCONUT OIL HAS THE ADVANTAGE THAT IT CONSTITUENTS ( LAURIC ACID AND MONOLAURIN , CAPRIC ACID AND MONOCAPRIN ) LOOKS TO HAVE ANTIBACTERIAL , ANTIVIRAL AND ANTIFUNGAL PROPIERTIES , just against the microbes (virus as herpes simplex , spirochaete (as Borrelia) , Chlamydia and fungi) ,described in the very important editorial of the Journal of Alzheimer Disease .Then, extra virgin coconut oil can be studied by researchers as a PREVENTION AND/OR AS SUPPORT THERAPY against infections with such microbes in AD , as we can see in the reference articles bellow :
    1) Coconut oil constituents as a support therapy against Lyme disease : IN VITRO EVALUATION OF ANTIBACTERIAL ACTIVITY OF PHYTOCHEMICALS AND MICRONUTRIENTS AGAINST BORRELIA BURGDORFERI AND BORRELIA GARINII. J Appl Microbiol. 2015-Goc A and colleagues
    2) Coconut oil constituents as a support therapy against Helicobacter Pylori – ANTIBACTERIAL ACTIONS OF FATTY ACIDS AND MONOGLYCERIDES AGAINST HELICOBACTER PYLORI – Immunol Med Microbiol. 2003 3) Coconut oil constituents as a support therapy against Herpes – DEVELOPMENT AND EVALUATION OF MICROBICIDAL HYDROGELS CONTAINING MONOGLYCERIDE AS THE ACTIVE INGREDIENT. – Kristmundsdóttir T – J Pharm Sci. 1999
    5) IN VITRO INACTIVATION OF CHLAMYDIA TRACHOMATIS BY FATTY ACIDS AND MONOGLYCERIDES – Bergsson G and colleagues -.J. Antimicrob Agents Chemother.1998

  4. The findings that AD has a microbial etiology is indeed a significant finding. Microbiologists can possibly try using probiotics for the prevention and treatment of AD. Recent research outputs have shown that the human intestinal microbiome composition plays an important role in orchestrating the overall health and well-being of an individual. Probiotics have already been used for the prevention of certain nutritional deficiencies, hyperlipidemia, colorectal cancer and hopefully even diabetes.

  5. I wonder though, some AD patients must have been receiving antibiotics for infections they get, has anyone ever gotten better after receiving such antibiotics?

    1. This may be a situation where the infecting/offending organism does the damage to start the process in motion and once established antimicrobial therapy is not effective. Examples include Hepatitis C or B virus where treated early causes limited liver damage but over time may lead to cirrhosis or liver cancer. At that later time treating the virus is too late. Trials might want to focus on very early AD or better yet if one can make the definite link between an organism and AD treat before symptoms develop. As a microbiologist I believe it warrants much more study.

  6. This is sad to read these comments as they are true I’ve watched Dr’s do this to all my grandparents over the years and then a veteran neighbor who died from agent orange :( first thing hospice did was put him on halidol I couldn’t figure a reason besides ugh well he went fast I pray they slow this down

  7. It was never AD…..My thoughts think more like 3rd stage syph…Give them all I.V. penicillin for the prescribed course for that disease and see how many AD and dementia cases have a miraculous recovery.

  8. Two Spriochetal Infections, Borrelia spirochetes ( Blood and Tissue pathogens) Transmitted by insect bites, and Treponemal spirochetes from the oral cavity ( Periodontal disease pathogens) are linked to Alzheimer’s Disease

    I offer in support of the Chronic Borrelia spirochete brain infections in Alzheimer’s disease, the following two links
    to lectures which describe images of he Borrelia in Autopsy Alzheimer’s Brain tissue from the Harvard Medical School Brain Bank.

    Link:; Original 37 min Powerpoint without narration:

    Link:: Video with Narration 44 min.:
    Final Lecture German Borreliosis Society Alan B MacDonald Lecture March 11 2016

    Borrelia brain infections provide he most Photographic documentation of The Cause of Alzheimer’s Disease, as proven by direct Photographs of these microbes by DNa probe imaging in autopsy Alzheimer’s disease Brains.


    Alan B. MacDonald, MD
    Fellow, College of American Pathologists
    President and CEO, the Dr. Paul H Duray Research Fellowship Endowment, Inc.

  9. Nursing homes that have a dementia or alzheimers unit actually lose money. They tend to have people there the longest and for general maintenance, not higher paid skilled nursing procedures. As a nurse on a dementia unit, I can’t imagine that anyone that actually met someone with advanced dementia would only think of that person in terms of how much money they could make off of them. But, unfortunately, it does happen.

  10. As ApoE4 genotype has been linked to weakened blood-brain-barrier, this article may explain how this genotype predisposes to AD, by allowing ‘bugs’ to enter brain. Interesting…

  11. It is an intriguing idea. We know that Chicken Pox reemerges as shingles. Go into this further and see if it is a possible dormant virus etc.

  12. Very interesting. My mom passed away about a year ago from kidney failure and advanced Alzheimer’s. I know her medical history is in line with the theories in this article. I have Klippel-Feil syndrome and progressive neurologic symptoms, and along with that memory issues which keep me in fear of meeting the same end. However, Alzheimer’s is big business, generating billions via medications, nursing homes, adult day care, and other services. I can see where traditional medicine would fight this research.

  13. Though not yet published, US researcher Dr. Alan MacDonald, (who published evidence of a spirochaete-Alzheimer’s link as long ago as the 1980s), has recently detected the specific DNA of Borrelia burgdorferi and Borrelia miyamotoi bacteria in the autopsy brain tissue of Alzheimer victims, as well as one patient with Lewy Body Dementia.

    This was achieved with Molecular beacon DNA probes, highly accurate probes which will not hybridise if even a single nucleotide is mis-matched.

    Please see and for more details.

    E. Cook
    Board Member,
    Spirochaetal Alzheimer’s Association (SAA)

  14. This is an interesting article. I think fundings for the clinical trials should be instituted in other to proof or disproof this relationship between infection and AD. There have been many funded clinical trials on AD and other concepts which showed little or no evidence. So i see no reason why this concept should not also be funded for clinical trials. For as it is realised, the promising concepts are the ones which are always initially rejected and they only come to realise it many years later. For example, the idea of the scientist who said peptic ulcer was caused by a bacterium was rejected until he had to proved it himself by drinking a cork-tail of the bacterium which is not suppose to be that way.

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