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.
This
major call for action is based on substantial published evidence into
Alzheimer’s. Image is adapted from the University of Manchester press
release.
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
Abstract
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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