Assessment of evidence for or against contributions of Chlamydia pneumoniae infections to Alzheimer’s disease etiology
•Chlamydia pneumoniae found at increased rates in the brain in Alzheimer’s disease.•Limitations of past human and animal studies prevent conclusive interpretation.•The mouse pathogen Chlamydia muridarum may help investigate pathogenesis.•Better validation of amyloid-like deposits in mouse infection...
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Published in | Brain, behavior, and immunity Vol. 83; pp. 22 - 32 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Netherlands
Elsevier Inc
01.01.2020
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Subjects | |
Online Access | Get full text |
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Summary: | •Chlamydia pneumoniae found at increased rates in the brain in Alzheimer’s disease.•Limitations of past human and animal studies prevent conclusive interpretation.•The mouse pathogen Chlamydia muridarum may help investigate pathogenesis.•Better validation of amyloid-like deposits in mouse infection models is needed.•Resolving these issues is important for reproducibility and clearer understanding.
Alzheimer’s disease, the most common form of dementia, was first formally described in 1907 yet its etiology has remained elusive. Recent proposals that Aβ peptide may be part of the brain immune response have revived longstanding contention about the possibility of causal relationships between brain pathogens and Alzheimer's disease. Research has focused on infectious pathogens that may colonize the brain such as herpes simplex type I. Some researchers have proposed the respiratory bacteria Chlamydia pneumoniae may also be implicated in Alzheimer’s disease, however this remains controversial. This review aims to provide a balanced overview of the current evidence and its limitations and future approaches that may resolve controversies. We discuss the evidence from in vitro, animal and human studies proposed to implicate Chlamydia pneumoniae in Alzheimer’s disease and other neurological conditions, the potential mechanisms by which the bacterium may contribute to pathogenesis and limitations of previous studies that may explain the inconsistencies in the literature. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 |
ISSN: | 0889-1591 1090-2139 |
DOI: | 10.1016/j.bbi.2019.10.014 |