A century ago, Alois Alzheimer and his colleagues suggested that microorganisms likely contribute to the generation of senile plaques in patients with the disease that now bears his name. Apparently few people listened, as over the past decades, research on Alzheimer’s disease has focused almost soley on searching for a genetic cause of the illness. As reported by Science Daily, “The fact that pathogens may suppress, subvert or evade host defenses and establish chronic or latent infection [in Alzheimer’s] has received little attention in the past, despite the fact that during infection, active oxygen and nitrogen species generated by inflammatory cells may cause DNA damage, induce apoptosis, and modulate enzyme activities and gene expression.”

However, since those scientists fixated on finding a genetic cause for Alzheimer’s have yet to correlate particular genes with the disease, an increasing number of other research teams are beginning to search for alternative causes of the illness. Happily, this new streak of research focuses on the role of bacteria in causing the Alzheimer’s.

For example, In a special issue of the Journal of Alzheimer’s Disease published May 2008, guest editors Judith Miklossy, from The University of British Columbia, and Ralph N. Martins, from Edith Cowan University and Hollywood Private Hospital, Perth, Western Australia, explore the role of bacteria in causing Alzheimer’s.

The issue, which consists of a series of reviews, draws attention to both historic and recent observations related to this emerging field of Alzheimer’s research. Although the teams do implicate bacteria as possible causal agents of Alzheimer’s, they still focus on a “one pathogen, one disease” hypothesis. However, those people familiar with the work of biomedical researcher Trevor Marshall understand that Alzheimer’s is not caused by a single pathogen. Rather, Marshall’s in silico and clinical data has made it clear that inflammatory diseases like Alzheimer’s result from infection with an wide array of chronic intraphagocytic bacteria that persist inside biofilms as well as inside the nuclei of the cells they infect.

Yet, it’s still a breath of fresh air that more Alzheimer’s research teams are at least headed down the right path. The first review article accurately stresses the importance of chronic inflammation in Alzheimer’s. A second review is also on the right track in the sense that it discusses a possible correlation between higher levels of pathogenic bacteria in the mouth and the prevalence of Alzheimer’s. Since chronic intraphagocytic bacteria in the mouth likely create substances that block the VItamin D Receptor and subsequently the innate immune response, the team is correct in concluding that the presence of chronic pathogens in one area of the body can facilitate the spread of different chronic pathogens in other areas of the body, such as the brain.

Also, few MP-minded individuals would disagree with Miklossy and Martins statement that, “The historic and new observations reviewed in this special issue clearly show that high priority should be given for further research in this field as it may have major implications for public health, treatment, and prevention as adequate anti-bacterial and anti-viral drugs are available. The impact on reducing healthcare costs would be substantial.”

Yes, it would. That’s why it will be exciting when Miklossy and Martins become acquainted with the Marshall Protocol. Although no patient with Alzheimer’s has completed the treatment, patients with a range of other inflammatory mental illnesses such as ADD, OCD, bipolar disorder, depression, and general brain fog and memory loss are reporting improvement and recovery. It hard to image that Alzheimer’s won’t follow the same trend.