Affiliations: [a] School of Animal Science, Louisiana State University Agricultural Center, Baton Rouge, LA, USA
| [b]
Tulane Medical School, New Orleans, LA, USA
| [c]
Texas Tech University, Lubbock, TX, USA
Correspondence:
[*]
Correspondence to: Frank O. Bastian, MD, Professor of Animal Science, LSU Agricultural Center, Baton Rouge, LA 70803, USA. E-mail: [email protected].
Abstract: The question whether Alzheimer’s disease is infectious as brought up in the recent editorial published in the Journal of Alzheimer’s Disease is complicated by the controversy whether the causal agent is a microbe or a misfolded host protein (amyloid). The replicating amyloid (prion) theory, based upon data from studies of Creutzfeldt-Jakob disease (CJD) and other transmissible spongiform encephalopathies (TSEs), has been challenged since the prion can be separated from TSE infectivity, and spiroplasma, a wall-less bacterium, has been shown to be involved in the pathogenesis of CJD. Further support for a microbial cause for AD comes from occurrence of mixed CJD/AD cases involving up to 15% of AD brains submitted to brain banks. The association of CJD with AD suggests a common etiology rather than simply being a medical curiosity. A co-infection with the transmissible agent of CJD, which we propose to be a Spiroplasma sp., would explain the diversity of bacteria shown to be associated with cases of AD.
