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The Infectious Etiology of Alzheimer s Disease
#MMPMID28294067
Sochocka M
; Zwoli?ska K
; Leszek J
Curr Neuropharmacol
2017[]; 15
(7
): 996-1009
PMID28294067
show ga
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.