Several researchers within the field of Alzheimer's disease (AD) expressed their opinion regarding the role of microbes in the development of the disease in the recent issue of the Journal of Alzheimer's Disease.
These voices cannot be ignored given that 33 professionals contributed, and these experts represent 10 different countries. The researchers from the United States included expertise from research groups in Arkansas, Michigan, New Mexico, New York, Oregon, Pennsylvania and Texas, and this wide geographical distribution indicates a universal concern.
The opinion review expressed an alarm and concern that, despite the hundreds of studies on humans indicating a role of microbes in the degeneration of the aging brain, the area of work remains largely ignored. They cited work related to infectious processes such the herpes simplex virus, chlamydia, pneumoniae, fungal infections and several types of spirochetes.
The authors point out we have long recognized that AD has a major inflammatory component. They also point out the most widely recognized risk factor for AD — the Apolipoprotein E gene — plays a role in modulating the immune system and the overall susceptibility to infectious disease processes.
An interesting observation that gives even greater credibility to the claim that microbes contribute to brain pathology is the hypothesis of a logical entry point for microbes. The editorial acknowledges that olfactory dysfunction is one of the earliest symptoms for AD.
The neural tissue related to smell is exposed to environment. The olfactory nerve goes directly to the brain regions that are the initial site of AD-related pathology. Thus, the nose is a likely entryway for many viruses.
Early and ongoing research has concentrated on understanding the deposits associated with AD in the brain, called amyloid plaques. It is now understood that infections with a virus can lead to these amyloid deposits. The amyloid plaques are now being seen as a response to microbes and may be a defense mechanism.
The investigation into microbes as a causative factor in AD is long overdue. The AD researchers suspect the delay has been caused by a bias against microbe theories that parallels those who doubted the contribution of viruses and bacteria to cancer and stomach ulcers. Such theories were eventually proven correct.
"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," Professor Resia Pretorius of the University of Pretoria in South Africa, who also worked on the editorial, told the Yorkshire Post.
This editorial points out an estimated 413 trials of different types of therapies to target the AD during the years of 2002 to 2012. All have failed. They propose targeting antiviral and antimicrobial treatment to AD patients, in particular those who have the Apolipoprotein E gene risk factors.
In response to the article, the editors of the Journal of Alzheimer's Disease offer these comments:
"Efforts worldwide to target amyloid as a cause of disease were an essential step along the path because they demonstrated that amyloid does not cause Alzheimer disease. Now it is time to move on and address whether combating microbes might provide respite for Alzheimer patients. It is very important to recognize that Alzheimer is not an infectious disease like chickenpox. All of us are persistently infected with infectious agents, such as herpes viruses, but these for the most part are silent. Only with aging and decline of the immune system do these become reactivated. But there are tools to combat proliferation, and several potent antimicrobial drugs are available. These now warrant testing in Alzheimer disease."
AD impacts the lives of patients, families and the caregiver community. While targeting microbes may not cure the disease, the strategy certainly warrants further investigation as it shows promise in mitigating the symptoms of the disease.
