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 inBrain, behavior, and immunity Vol. 83; pp. 22 - 32
Main Authors Woods, Jason J., Skelding, Kathryn A., Martin, Kristy L., Aryal, Ritambhara, Sontag, Estelle, Johnstone, Daniel M., Horvat, Jay C., Hansbro, Philip M., Milward, Elizabeth A.
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier Inc 01.01.2020
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Abstract •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.
AbstractList 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.
•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.
Author Hansbro, Philip M.
Martin, Kristy L.
Aryal, Ritambhara
Johnstone, Daniel M.
Horvat, Jay C.
Milward, Elizabeth A.
Woods, Jason J.
Skelding, Kathryn A.
Sontag, Estelle
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Keywords Infection
Prevention
Brain
Chlamydia pneumoniae
Immune response
Treatment
Alzheimer’s disease
Risk factor
Inflammation
Chlamydia muridarum
Language English
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Snippet •Chlamydia pneumoniae found at increased rates in the brain in Alzheimer’s disease.•Limitations of past human and animal studies prevent conclusive...
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...
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StartPage 22
SubjectTerms Alzheimer Disease - etiology
Alzheimer Disease - microbiology
Alzheimer’s disease
Animals
Brain
Brain - microbiology
Chlamydia muridarum
Chlamydia pneumoniae
Chlamydophila Infections - complications
Chlamydophila Infections - microbiology
Chlamydophila pneumoniae - pathogenicity
Humans
Immune response
Infection
Inflammation
Prevention
Reproducibility of Results
Risk factor
Treatment
Uncertainty
Title Assessment of evidence for or against contributions of Chlamydia pneumoniae infections to Alzheimer’s disease etiology
URI https://dx.doi.org/10.1016/j.bbi.2019.10.014
https://www.ncbi.nlm.nih.gov/pubmed/31626972
https://search.proquest.com/docview/2307128332
Volume 83
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