For years the cause of Alzheimer’s disease has been up for debate.
Is it natural degeneration due to aging? Perhaps this plays a part, but not everyone gets it.
Do genetics dictate who’s more susceptible?
And certainly we can’t ignore the research that points to a correlation between Alzheimer’s and exposure to environmental toxins or diets high in sugar consumption.
Clearly, scientists have yet to fully understand the cause and progression of Alzheimer’s and other forms of dementia. And that leaves us without a probable cure or guaranteed preventative tactics.
And a new perspective on the radar brings another possibility of disease causality to the table. In March 2016, an editorial was published in the Journal of Alzheimer’s Disease, expressing concern over one aspect of the disease that has been largely neglected.
A community of Alzheimer’s disease researchers and clinicians are prepared to back up their belief that certain pathogenic microbes in the elderly brain have strong correlations to Alzheimer’s.
What pathogens have been implicated in the development of Alzheimer’s?
- Herpes simplex virus type 1 (HSV1): This virus is responsible for oral herpes that cause cold sores and fever blisters to form around the mouth and on the face.
- Chlamydia pneumoniae: This bacteria can cause lung infections, such as pneumonia.
- Spirochetes: Several members of this family of bacteria are also under suspicion.
The panel of scientists is pushing for more concentrated research on the microbial effect on Alzheimer’s based on findings from hundreds of studies with more than 100 studies on HSV1 alone, a concept that was first observed roughly 30 years ago.
A separate theory regarding Alzheimer’s disease may be a link to the microbial aspect and the long-held view that the disease is caused by sticky plaques made of amyloid proteins.
A Harvard research group published a study in the May 2016 issue of the journal Science Translational Medicine. Their findings revealed that the presence of pathogenic bacteria in the brain may encourage the formation of beta-amyloid plaque as a response to fighting a bacterial infection.
Researchers hypothesized that when an offending microbe crosses the blood-brain barrier, the immune response is to send the brain’s amyloid proteins (normal components of the brain’s protein matrix) to trap the organism and suppress infection, similar to how proteins surround pathogens elsewhere in the body before white blood cells swoop in to finish the job to stop infection.
However, the build-up of such proteins into plaques near the hippocampus, where learning and memory take place, supports one of the current beliefs in the cause of Alzheimer’s – that amyloid plaques form and encourage the tangling of tau proteins, which kills nerve cells and initiates inflammation that kills even more nerve cells. Essentially, the brain wastes away.
Researchers across the board agree that there’s much more work to be done regarding the brain’s innate immune system and whether it’s actually contributing to Alzheimer’s in some individuals.
But as with many controversial theories regarding diseases, proposals to fund the necessary clinical trials are often denied, which hinders successful trials that could pave the way for the development of appropriate prevention and treatment protocols.
If allowed to be fully explored and recognized as a valid cause of Alzheimer’s disease, it raises the question whether similar theories about microbial infections have implications in the treatment of other progressive neurological diseases like Parkinson’s.
This could turn out to be another reason to give your best effort in preventing bacterial and viral infections.