For a century it has been known that the chronic bacterial infections, namely Treponema pallidum (a form of geral paresis in syphilis), is the most frequent cause of dementia. Alois Alzheimer suggested a century ago that microorganisms may be contributors in the generation of Alzheimer’s disease plaques.
A special May issue of the Journal of Alzheimer’s Disease, 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, and a group of experts explore the topic of how pathogens may suppress, subvert or evade host defenses and establish chronic or latent infection, which has received little attention in the past.
It appears that during an infection cells generated by inflammatory cells may cause DNA damage. Depending upon the biology of the pathogen and the host defense mechanisms the organism can persist in the infected tissues and cause chronic inflammation and amyloid plaque. The outcome of infection is as much determined by the genetic predisposition of the patient as by the virulence and biology of the infecting agent.
This special issue contains a series of reviews from both a historical and recent perspective. The first review shows the importance of chronic inflammation in AD, followed by three articles presenting evidence on the involvement of spirochetes, Chlamydia pneumonia and Herpes simplex virus type 1 in Alzheimer’s disease. These are followed by a review of amyloid proteins, which occur in many cellular forms in Eukaryotes and Prokaryotes.
The editors feel that treatment of a bacterial infection and associated viral infection may result in regression and, if started early, prevention of disease. The impact on reducing health-care costs would be substantial.