A journal paper by over 30 researchers and clinicians says that in the light of the ever-increasing number of studies implicating microbes in Alzheimer’s disease, it is time to re-evaluate the idea of infection as a cause of the neurodegenerative disorder.
In an editorial in the Journal of Alzheimer’s Disease, the experts say they are concerned that mainstream research appears to be neglecting the idea that microbes could be a cause of Alzheimer’s disease – even though treatment based on it might slow or arrest the disease.
They refer in particular to evidence linking the development of Alzheimer’s disease (AD) to three microbes: the virus that causes cold sores – herpes simplex virus type 1 (HSV1) – chlamydia bacteria and a type of corkscrew-shaped bacteria called spirochaete. They note:
“The ever-increasing number of these studies (now about 100 on HSV1 alone) warrants re-evaluation of the infection and AD concept.”
The authors, including experts from the Universities of Oxford, Cambridge, Manchester and Edinburgh in the UK, say the abundant data implicating microbes in the development of Alzheimer’s has been largely ignored or dismissed as controversial.
Also, they note how proposals for clinical trials to follow up on this evidence have been refused – despite the fact that over the last 10 years we have observed the failure of over 400 clinical trials testing more accepted theories of Alzheimer’s.
The experts liken the opposition to the ideas they propose to the fierce resistance that met many studies that showed cancer could arise from viruses or that bacteria could cause stomach ulcers – ideas since proved to be correct in clinical trials and the development of subsequent new treatments.
The authors want to see more attention given to the idea that microbes find their way into the brain via the bloodstream and lie dormant until triggered by aging, immune system decline or by different types of stress.
Once they are activated, the microbes then damage brain cells – either directly or via inflammation. This approach also suggests beta-amyloid – the faulty protein that is found in the brains of people with Alzheimer’s disease – is not a primary cause of disease but “initially, appears to be only a defense mechanism,” note the editorial authors.
One of the authors, Douglas Kell, a professor at Manchester University’s School of Chemistry and also of the Manchester Institute of Biotechnology, says there is evidence of dormant microbes hiding in what was thought to be sterile red blood cells – a finding that has implications for blood transfusions. He describes the trigger mechanism:
“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.”
Another editorial author, Prof. Resia Pretorius, of the University of Pretoria in South Africa, adds:
“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.”
Prof. Pretorius says there is also evidence that this can lead to brain inflammation and the beta-amyloid plaques seen in Alzheimer’s disease.
The authors note that the ideas and findings they mention could also have implications for Parkinson’s disease and other brain-wasting conditions.
There has been a mixed reaction to the paper. Dr. James Pickett, head of research at the UK-based Alzheimer’s Society, acknowledges that many viruses, bacteria and fungi found in the brains of older people appear to be more prevalent in the brains of those who die with Alzheimer’s disease. But he notes:
“While these observations are interesting and warrant further research, there is currently insufficient evidence to tell us that microbes are responsible for causing Alzheimer’s disease in the vast majority of cases.”
He says the charity would like to reassure people there “remains no convincing evidence that Alzheimer’s disease is contagious or can be passed from person to person like a virus.”
He adds that the charity welcomes research into all possible causes of dementia and that improves diagnosis, treatment and prevention of the disease.
The reaction of other Alzheimer’s experts is less guarded. John Hardy, a professor of neuroscience at University College London, UK, suggests most researchers working on Alzheimer’s disease would not agree with the editorial. He is reported by various media as saying:
“This is a minority view in Alzheimer research. There had been no convincing proof of infections causing Alzheimer disease. We need always to keep an open mind but this editorial does not reflect what most researchers think about Alzheimer disease.”
Meanwhile, Medical News Today recently learned about a study that shows an already approved anti-cancer drug could delay the onset of Alzheimer’s disease.