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Editorial
. 2022 May-Jun;44(3):245-247.
doi: 10.1590/1516-4446-2021-0037.

What is the role of microbial infection in Alzheimer's disease?

Tatiana Barichello  1   2 , Vijayasree V Giridharan  1 , Clarissa M Comim  3 , Rodrigo Morales  4   5
Affiliations
Editorial

What is the role of microbial infection in Alzheimer's disease?

Tatiana Barichello et al. Braz J Psychiatry. 2022 May-Jun.
No abstract available

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Conflict of interest statement

The authors report no conflicts of interest.

Figures

Figure 1
Figure 1. Kaplan-Meier survival curve of APP/PS1 mice, WT C57BL/6 mice, and Wistar rats subjected to experimental polymicrobial sepsis triggered by CLP. Control groups subjected to sham surgery were included for comparison. The animals were followed for 10 days and mortality was recorded (APP/PS1, sepsis n=32 vs. control n=16, p = 0.153; C57BL/6 mice, sepsis n=50 vs. control n=50, p < 0.001; Wistar rats, sepsis n=12 vs. control n=10, p = 0.02). The APP/PS1 mice subjected to sepsis had an 87.88% survival rate, WT mice had a survival rate of 56%, and Wistar rats had a survival rate of 58.33%. APP/PS1 = amyloid-β precursor protein/presenilin 1; CLP = cecal ligation and puncture.
Figure 2
Figure 2. Infection-induced inflammation as a potential trigger of Alzheimer’s disease pathology. Infection or inflammation activates microglial cells, triggering the release of pro-inflammatory cytokines. In sequence, the pro-inflammatory cytokines promote the formation of interferon-induced transmembrane protein 3 (IFITM3) in neurons and astrocytes, which binds to γ-secretase, increasing its activity and upregulating Aβ production. Released Aβ peptides have antimicrobial effects, preventing pathogen development by forming amyloid plaques. Brain Aβ deposition exacerbates the cerebral inflammatory response, accelerating AD pathological cascades. Aβ = amyloid-β; AD = Alzheimer’s disease.
See this image and copyright information in PMC

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