It has been known from a century that chronic bacterial infections are frequently associated with amyloid deposition and that experimental models of inflammation and amyloidosis can be produced by injecting living or killed bacteria or their toxic components to animals. It has also been known from a century that chronic bacterial infection can cause dementia. Treponema pallidum, the causative agent of syphilis, causes slowly progressive dementia, cortical atrophy, chronic inflammation and amyloid deposition in the affected brain.
Alzheimer’s disease (AD), the most frequent cause of dementia, is a form of amyloidosis. The pathological mechanisms driving the accumulation of amyloid remain unclear. Bacteria, including spirochetes, are powerful stimulators of inflammation and are amyloidogenic. They were suggested to be contributors in generating and sustaining chronic inflammation and amyloid deposition in Alzheimer’s disease. The concept is not new. Fischer, Alzheimer and their colleagues have discussed the possibility that microorganisms may play a role in senile plaque formation already century ago.

The results of all these studies when taken together allow us to conclude that Borrelia burgdorferi and oral spirochetes can persist in the brain and in analogy to Treponema pallidum, can cause chronic or late neurospirochetoses and cause dementia, cortical atrophy and amyloid deposition. Exposure to spirochetesa or to their toxic products, host responses similar in nature to those observed in AD may be induced. Spirochetes together with other bacteria and viruses may initiate a cascade of events leading to cell death, neurodegeneration and amyloid deposition in AD. In a similar way microorganisms, including various types of spirochetes, including oral, intestinal and several Borrelia species, as well as other bacteria, like Chlamydia pneumoniae, Helicobacter pylori and yet uncharacterized coccoid and fusiform, bacteria and viruses might initiate chronic inflammation and amyloid deposition in type 2 diabetes, in atherosclerosis and in many other chronic inflammatory disorders. As a consequence they may cause tissue atrophy, amyloid deposition and cellular death and dysfunction.

The fact that pathogens may suppress, subvert or evade host defenses and establish chronic or latent infection has received little attention in the past. During infection, active oxygen and nitrogen species generated by inflammatory cells can cause DNA damage, induce apoptosis, and modulate enzyme activities and gene expression. Depending upon the biology of the pathogen and the host defense mechanisms the microorganisms can persist in the infected tissues, resulting in chronic, persistent inflammation. 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. Environmental factors, including stress and nutrition are critical determinants of disease expression as well.

Pathogens, in addition to strong lymphoplasmocytic infiltrates, can also induce slowly progressive chronic inflammation with poor or absent lymphoplasmocytic infiltrates (e.g. leprosy, syphilis). Activated macrophages and/or microglia are the principal players in this slowly progressive form of infection, which results in slowly progressive parechymal involvement and tissue atrophy.

Highest priority should be given to this emerging field of research. It may have major implications for public health, in the treatment, and prevention of Alzheimer disease and other associated chronic inflammatory disorders as adequate anti-bacterial drugs are available. Treatment of a bacterial infection may result in regression and, if started early, prevention of the disease. The impact on reducing health-care costs would be substantial.

As it was the case for paretic dementia in syphilis, one may prevent and eradicate dementia in Alzheimer disease.