Can We Have a Unified Microbiome Initiative? Yours, the microbiologists.”
As it happens, the answer is yes.
Today, the White House is announcing the launch of the National Microbiome Initiative (NMI)—an ambitious plan to better understand the microbes that live in humans, other animals, crops, soils, oceans, and more. These miniscule organisms are attracting mammoth budgets: federal agencies are committing $121 million to the NMI over the next two years, while more than 100 universities, non-profits, and companies are chipping in another $400 million.
Essentially, America has decided to point half a billion microscopes at the planet, and look through them.
There is a clear-cut need for a new approach to solve the problem of Alzheimer's disease. If we do not know the cause of the disease, we will soon face a health care crisis as the number of patients suffering from Alzheimer's disease continuously increases.
Increasing number of physicians and scientists claim that an infectious origin of Alzheimer's disease cannot be more neglected as expressed in an editorial of the Journal of Alzheimer's disease.
In-Depth-Telegraph.co.uk-Mar 8, 2016
Benzinga-May 13, 2016
Increasing number of observations show that type 2 diabetes, similarly to Alzheimer's disease is caused by chronic bacterial infection.
Strong epidemiologic evidence and common molecular mechanisms support an association between Alzheimer's disease (AD) and type 2-diabetes. Local inflammation and amyloidosis occur in both diseases and are associated with periodontitis and various infectious agents. This article reviews the evidence for the presence of local inflammation and bacteria in type 2 diabetes and discusses host pathogen interactions in chronic inflammatory disorders. Chlamydophyla pneumoniae, Helicobacter pylori and spirochetes are demonstrated in association with dementia and brain lesions in AD and islet lesions in type 2 diabetes. The presence of pathogens in host tissues activates immune responses through Toll-like receptor signaling pathways. Evasion of pathogens from complement-mediated attack results in persistent infection, inflammation and amyloidosis. Amyloid beta and the pancreatic amyloid called amylin bind to lipid bilayers and produce Ca(2+) influx and bacteriolysis. Similarly to AD, accumulation of amylin deposits in type 2 diabetes may result from an innate immune response to chronic bacterial infections, which are known to be associated with amyloidosis. Further research based on an infectious origin of both AD and type 2 diabetes may lead to novel treatment strategies.
See also a related article
Type 2 Diabetes: Local Inflammation and Direct Effect of Bacterial Toxic Components Judith Miklossy*,1, Ralph Martins2, Nune Darbinian3, Kamel Khalili3 and Patrick L. McGeer1 http://www.miklossy.ch/media/Miklossy_OPATJ.pdf
All the clinical, pathological and biological hallmarks, which define Alzheimer's disease, have been reported and illustrated by hundreds of other authors, indicating that chronic spirochetal infection can cause Alzheimer's dementia.
Prevention Alzheimer International Foundation, International Alzheimer Research Center, Martigny-Croix, Switzerland
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. To answer this question, observations and illustrations on the detection of spirochetes in the atrophic form of general paresis, which is known to be associated with slowly progressive dementia, were reviewed and compared with the characteristic pathology of AD. 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. Cortical spirochetal colonies are made up by innumerable tightly spiraled Treponema pallidum spirochetes, which are morphologically indistinguishable from senile plaques, using conventional light microscopy. Local brain amyloidosis also occurs in general paresis and, as in AD, corresponds to amyloid beta. 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.
The End of Alzheimer's?: A Differential Diagnosis Toward a Cure
with forewords by Kilmer McCully and Jack C. de la Torre
It is strongly recommended to read this excellent book: It is strongly related to our goals
Some comments about the involvement of spirochetes in Alzheimer's disease.
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
On 13 Aug, 2014