ArticleActa neuropathologica2007
Detection of amyloid beta aggregates in the brain of BALB/c mice after Chlamydia pneumoniae infection.
Article in Acta neuropathologica, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
22 citing papers in PubMed, 38 citations in OpenAlex.
- Exploring the role of multi-pathogen infections in Alzheimer's disease: A case-control study.Virulence · 2025Article
- Microbial Trojan Horses: Virulence Factors as Key Players in Neurodegenerative Diseases.Molecules (Basel, Switzerland) · 2025Review
- Review
- The gut microbiome in Alzheimer's disease: what we know and what remains to be explored.Molecular neurodegeneration · 2023Review
- Chlamydia pneumoniae can infect the central nervous system via the olfactory and trigeminal nerves and contributes to Alzheimer's disease risk.Scientific reports · 2022Article
- Phagocytosis by Peripheral Glia: Importance for Nervous System Functions and Implications in Injury and Disease.Frontiers in cell and developmental biology · 2021Review
- Association Between Antibiotic Treatment ofFrontiers in aging neuroscience · 2021Article
- Can Control Infections Slow Down the Progression of Alzheimer's Disease? Talking About the Role of Infections in Alzheimer's Disease.Frontiers in aging neuroscience · 2021Review
- Activity of Alzheimer's γ-secretase is linked to changes of interferon-induced transmembrane proteins (IFITM) in innate immunity.Molecular neurodegeneration · 2020Article
- Chronic Inflammatory Diseases at Secondary Sites Ensuing Urogenital or PulmonaryMicroorganisms · 2020Review
- Article
- Characterization of Brain Dysfunction Induced by Bacterial Lipopeptides That Alter Neuronal Activity and Network in Rodent Brains.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- The Physiological Roles of Amyloid-β Peptide Hint at New Ways to Treat Alzheimer's Disease.Frontiers in aging neuroscience · 2018Review
- Review
- Genetic, Transcriptome, Proteomic, and Epidemiological Evidence for Blood-Brain Barrier Disruption and Polymicrobial Brain Invasion as Determinant Factors in Alzheimer's Disease.Journal of Alzheimer's disease reports · 2017Article
- The Chlamydia pneumoniae Adhesin Pmp21 Forms Oligomers with Adhesive Properties.The Journal of biological chemistry · 2016Article
- Amyloid-β peptide protects against microbial infection in mouse and worm models of Alzheimer's disease.Science translational medicine · 2016Article
- Microbes and Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2016Review
- Detection of bacterial antigens and Alzheimer's disease-like pathology in the central nervous system of BALB/c mice following intranasal infection with a laboratory isolate of Chlamydia pneumoniae.Frontiers in aging neuroscience · 2014Article
- Can infections cause Alzheimer's disease?Epidemiologic reviews · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuroinflammation, initiated by cerebral infection, is increasingly postulated as an aetiological factor in neurodegenerative diseases such as Alzheimer's disease (AD). We investigated whether Chlamydia pneumoniae (Cpn) infection results in extracellular aggregation of amyloid beta (Abeta) in BALB/c mice. At 1 week post intranasal infection (p.i.), Cpn DNA was detected predominantly in the olfactory bulbs by PCR, whereas brains at 1 and 3 months p.i. were Cpn negative. At 1 and 3 months p.i., extracellular Abeta immunoreactivity was detected in the brain of Cpn-infected mice but also in the brain of mock-infected mice and mice that were neither Cpn infected nor mock infected. However, these extracellular Abeta aggregates showed morphological differences compared to extracellular Abeta aggregates detected in the brain of transgenic APP751(SL)/PS1(M146L) mice. These data do not unequivocally support the hypothesis that Cpn infection induces the formation of AD-like Abeta plaques in the brain of BALB/c mice, as suggested before. However, future studies are required to resolve these differences and to investigate whether Cpn is indeed an etiological factor in AD pathogenesis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.