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Circulating Chlamydia Trachomatis Antigens in Subjects With Alzheimer's Disease
Steven Lehrer1, Peter H Rheinstein2
1Department of Radiation Oncology, Icahn School of Medicine at Mount Sinai, New York City, NY, U.S.A.; steven.lehrer@mssm.edu.
Background/Aim:
Chlamydia pneumoniae (C. pneumoniae) is implicated in the pathogenesis of Alzheimer's disease (AD). Chlamydial elementary and reticulate bodies have been identified in tissues from afflicted AD brain regions by electron and immunoelectron microscopy, whereas similar tests of non-AD brains were negative for the bacterium. Studies in mice have shown that C. pneumoniae can rapidly penetrate the central nervous system by entering glia and causing beta amyloid deposition via the nerves between the nasal cavity and the brain, which serve as invasion pathways.
Materials And Methods:
We used data from the UK Biobank (UKBB) to assess the relationship of chlamydia and AD. Circulating C. pneumoniae antigen measurements were not available, but UKBB data field 23037 held measurements of PorB antigen for Chlamydia trachomatis (C. trachomatis). We used C. trachomatis as a surrogate for C. pneumoniae since serum cross-reactivity to C. trachomatis and C. pneumoniae antigens occurs in patients with documented infection and in healthy children as revealed by microimmunofluorescence and immunoblotting techniques. Single nucleotide polymorphism (SNP) data for rs429358 and rs7412 were used to impute ApoE genotypes.
Results:
PorB antigen levels for C. trachomatis were significantly higher in subjects with AD (p=0.007). PorB antigen levels were not related to ApoE genotype (e3e3, e3e4, e4e4) p=0.783. To control for the effects of age, sex, educational level, and apoE genotype, logistic regression analysis was performed. AD was the dependent variable. Independent variables were sqrt PorB antigen for C. trachomatis, age, sex, educational level, apoE genotype. AD odds ratio (OR) increased 1.156 for each unit increase of sqrt PorB antigen for C. trachomatis and the effect was significant (p=0.004).
Conclusion:
PorB antigens for C. trachomatis being significantly higher in subjects with AD, corroborates previous studies demonstrating that C. pneumoniae inflammation appears to play a role in AD development. AD may result from the reactivation of embryologic processes and pathways silenced at birth. A trigger for the reactivation may be bacterial or viral infections. Further studies are warranted.
Insights
Chlamydia trachomatis PorB antigen levels were higher in Alzheimer's disease (AD) patients, suggesting a role for chlamydial infections in AD pathogenesis. This finding supports the link between C. pneumoniae and AD development.
Area of Science:
- Neuroscience
- Infectious Disease Epidemiology
Background:
- Chlamydia pneumoniae (C. pneumoniae) is a suspected contributor to Alzheimer's disease (AD) pathogenesis.
- Bacterial bodies have been found in AD brain tissue, but not in healthy brains.
- Mouse studies indicate C. pneumoniae can enter the central nervous system via nasal pathways, promoting beta-amyloid deposition.
Purpose of the Study:
- To investigate the association between chlamydial infection markers and Alzheimer's disease using UK Biobank data.
- To explore the relationship between C. trachomatis PorB antigen levels and AD, using C. trachomatis as a surrogate for C. pneumoniae due to cross-reactivity.
Main Methods:
- Utilized UK Biobank data, including Chlamydia trachomatis (C. trachomatis) PorB antigen levels (UKBB field 23037) and ApoE genotypes (rs429358, rs7412).
- Employed logistic regression to analyze the association between PorB antigen levels and AD, controlling for age, sex, education, and ApoE genotype.
Main Results:
- Significantly higher PorB antigen levels for C. trachomatis were observed in subjects with AD (p=0.007).
- Each unit increase in sqrt PorB antigen for C. trachomatis was associated with a 1.156 increased odds of AD (p=0.004).
- PorB antigen levels showed no significant relationship with ApoE genotype (p=0.783).
Conclusions:
- Elevated C. trachomatis PorB antigens in AD patients support the hypothesis that C. pneumoniae-induced inflammation contributes to AD development.
- Bacterial or viral infections may trigger the reactivation of dormant pathways implicated in AD.
- Further research is needed to elucidate the role of chlamydial infections in Alzheimer's disease.
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