COULD Alzheimer’s disease (AD) be caused in part by infection?
Evidence has gradually accumulated to suggest that this theory about the etiology of Alzheimer’s disease (AD) should be taken up more seriously. And the serious tone is evidenced now in a series of articles in a special May 2008 issue of the Journal of Alzheimer’s Disease as reported on ScienceDaily and EurekAlert! (Both ScienceDaily and EurekAlert have good summaries of the news, so I'm not attempting a summary here — just passing along the news.)
But hasn't public scientific discussion of AD centered primarily on the genetic bases for the disease, for which we have good accumulating evidence? (See e.g. Ertekin-Taner, 2007, below.) And doesn't the apparent genetic basis/susceptibility for AD rather contradict an infection-based theory about the causes of the disease?
Yes … and most definitely No. The approaches are quite compatible. After all, genetics can determine in no small part, for example, one’s susceptibility to certain types of infection. So a disease may have significant genetic and environmental components — essentially a diathesis-stress model of disease.
Moreover, roughly 95% of cases of AD are non-familial late-onset Alzheimer’s disease (LOAD), also called “sporadic” AD, which has a number of known genetic risk factors — but risk factors aren't the same as determinants of the disease. Somehow such risk factors interact with environmental factors (in the broad sense of that phrase) to ultimately determine the course (if any) of the disease.
The work on AD is exciting and our growing understanding of its causes inspires hope that we'll eventually be able to treat and prevent this awful affliction.
Ertekin-Taner, Nilüfer (2007). Genetics of Alzheimer’s disease: a centennial review. Neurologic Clinics, 25(3), 611–667.
Balin, B., Little, C. S., Hammind, C. J., Appelt, D. M., Whittum-Hudson, J. A., Gerard, H. C., & Hudson, A. P. (2008) Chlamydophila pneumoniae and the etiology of late-onset Alzheimer’s disease. Journal of Alzheimer’s Disease, 13(4), 371–380.
Hammer, N. D., Wang, X., McGuffie, B. A., & Chapman, M. R. (2008) Amyloids: Friend or Foe? Journal of Alzheimer’s Disease, 13(4), 407–419.
Itzhaki, R. F. & Wozniak, M. A. (2008) Herpes Simplex Virus Type 1 in Alzheimer’s disease: The Enemy Within. Journal of Alzheimer’s Disease, 13(4), 393–405.
KRamer, A. R., Dasanayeke, A., Craig, R. G., Glodzik-Sobanska, L., Bry, M., & de Leon, M. J. (2008) Alzheimer’s disease and peripheral infections: The possible contribution from periodontal infections, model and hypothesis. Journal of Alzheimer’s Disease, 13(4), 437–449.
Miklossy, J. & Martins, R. (2008) Preface: Chronic inflammation and amyloidogenesis in Alzheimer’s disease: The emerging role of infection. Journal of Alzheimer’s Disease, 13(4), 357.
Miklossy, J. (2008) Chronic inflammation and amyloidogenesis in Alzheimer's disease – role of spirochetes. Journal of Alzheimer’s Disease, 13(4), 381–391.
Schwab, C. & McGeer, P. L. (2008) Inflammatory Aspects of Alzheimer Disease and Other Neurodegenerative Disorders. Journal of Alzheimer’s Disease, 13(4), 359–369.
Scott, L. C., Hammind, C. J., MacIntyre, A., Balin, B. J., & Appelt, D. M. (2004) Chlamydia pneumoniae induces Alzheimer-like amyloid plaques in brains of BALB/c mice. Neurobiology of Aging, 25(4), 419–429.
Urosevic, N. & Martins, R. N. (2008) Infection and Alzheimer’s disease: The ApoE e4 connection and lipid metabolism. Journal of Alzheimer’s Disease, 13(4), 421–435.
Weinberg, E. D. & Miklossy, J. (2008) Iron withholding: a defense against disease. Journal of Alzheimer’s Disease, 13(4), 451–463.