Astrocytes infected with Chlamydia pneumoniae demonstrate altered expression and activity of secretases involved in the generation of β-amyloid found in Alzheimer disease

BMC Neuroscience
Zein Al-AtracheDenah M Appelt

Abstract

Epidemiologic studies strongly suggest that the pathophysiology of late-onset Alzheimer disease (AD) versus early-onset AD has environmental rather than genetic causes, thus revealing potentially novel therapeutic targets to limit disease progression. Several studies supporting the "pathogen hypothesis" of AD demonstrate a strong association between pathogens and the production of β-amyloid, the pathologic hallmark of AD. Although the mechanism of pathogen-induced neurodegeneration of AD remains unclear, astrocytes, a key player of the CNS innate immune response and producer/metabolizer of β-amyloid, have been implicated. We hypothesized that Chlamydia pneumoniae infection of human astrocytes alters the expression of the amyloid precursor protein (APP)-processing secretases, ADAM10, BACE1, and PSEN1, to promote β-amyloid formation. Utilizing immunofluorescent microscopy, molecular, and biochemical approaches, these studies explore the role of an intracellular respiratory pathogen, Chlamydia pneumoniae, as an environmental trigger for AD pathology. Human astrocytoma cells in vitro were infected with Chlamydia pneumoniae over the course of 6-72 h. The gene and protein expression, as well as the enzymatic activity of non-amyloidog...Continue Reading

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Citations

Jan 19, 2020·Journal of Neuroinflammation·Sibo ZhuXingdong Chen
Jan 5, 2021·Frontiers in Cardiovascular Medicine·Ahmad Aljohmani, Daniela Yildiz
Jul 27, 2021·Frontiers in Cellular Neuroscience·Sarah K LotzKristen E Funk

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Methods Mentioned

BETA
PCR
Assay
protein assay
BACE
confocal microscopy
ELISA

Software Mentioned

FIJI
Qiagen online
FluoView 1000

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