Title:The Infectious Etiology of Alzheimer’s Disease
Volume: 15
Issue: 7
Author(s): Marta Sochocka *, Katarzyna Zwolińska and Jerzy Leszek
Affiliation:
- Laboratory of Virology, Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Rudolfa Weigla 12, 53-114 Wroclaw,Poland
Keywords:
Alzheimer’s Disease, neuroinflammation, chronic bacterial infections, chronic viral infections, neuroinfection,
neurotropic viruses.
Abstract: Background: Inflammation is a part of the first line of defense of the body against
invasive pathogens, and plays a crucial role in tissue regeneration and repair. A proper inflammatory
response ensures the suitable resolution of inflammation and elimination of harmful stimuli, but
when the inflammatory reactions are inappropriate it can lead to damage of the surrounding normal
cells. The relationship between infections and Alzheimer’s Disease (AD) etiology, especially lateonset
AD (LOAD) has been continuously debated over the past three decades.
Methods: This review discusses whether infections could be a causative factor that promotes the
progression of AD and summarizes recent investigations associating infectious agents and chronic
inflammation with AD. Preventive and therapeutic approaches to AD in the context of an infectious
etiology of the disease are also discussed.
Results: Emerging evidence supports the hypothesis of the role of neurotropic viruses from the
Herpesviridae family, especially Human herpesvirus 1 (HHV-1), Cytomegalovirus (CMV), and
Human herpesvirus 2 (HHV-2), in AD neuropathology. Recent investigations also indicate the
association between Hepatitis C virus (HCV) infection and dementia. Among bacteria special
attention is focused on spirochetes family and on periodontal pathogens such as Porphyromonas
gingivalis or Treponema denticola that could cause chronic periodontitis and possibly contribute to
the clinical onset of AD.
Conclusion: Chronic viral, bacterial and fungal infections might be causative factors for the
inflammatory pathway in AD.
