ReviewFrontiers in aging neuroscience2018
Review in Frontiers in aging neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
51 citing papers in PubMed, 78 citations in OpenAlex.
- Can we refute a role for infections in Alzheimer's disease pathogenesis?Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Unmasking the hidden catalyst: How infections trigger Alzheimer's disease.Journal of Alzheimer's disease : JAD · 2026Review
- Identification of Chlamydia pneumoniae and NLRP3 inflammasome activation in Alzheimer's disease retina.Nature communications · 2026Article
- Pyocyanin reversibly inhibitsFrontiers in pharmacology · 2026Article
- Seroprevalence ofPathogens (Basel, Switzerland) · 2025Article
- Infections withFrontiers in aging neuroscience · 2025Review
- The Chlamydia pneumoniae effector SemD exploits its host's endocytic machinery by structural and functional mimicry.Nature communications · 2024Article
- Clinically apparent Helicobacter pylori infection and the risk of incident Alzheimer's disease: A population-based nested case-control study.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- New approaches for understanding the potential role of microbes in Alzheimer's disease.Brain, behavior, & immunity - health · 2024Review
- MAD-microbial (origin of) Alzheimer's disease hypothesis: from infection and the antimicrobial response to disruption of key copper-based systems.Frontiers in neuroscience · 2024Review
- Review
- Vaccines and Dementia: Part II. Efficacy of BCG and Other Vaccines Against Dementia.Journal of Alzheimer's disease : JAD · 2024Review
- Establishment of a consensus protocol to explore the brain pathobiome in patients with mild cognitive impairment and Alzheimer's disease: Research outline and call for collaboration.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023Review
- Neuroinflammation in Alzheimer's Disease: A Potential Role of Nose-Picking in Pathogen Entry via the Olfactory System?Biomolecules · 2023Review
- Clinical evidence of human pathogens implicated in Alzheimer's disease pathology and the therapeutic efficacy of antimicrobials: an overview.Translational neurodegeneration · 2023Review
- A single chlamydial protein reshapes the plasma membrane and serves as recruiting platform for central endocytic effector proteins.Communications biology · 2023Article
- Friends and Foes in Alzheimer's Disease.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2023Review
- AGE-RAGE axis culminates into multiple pathogenic processes: a central road to neurodegeneration.Frontiers in molecular neuroscience · 2023Review
- The electronic tree of life (eToL): a net of long probes to characterize the microbiome from RNA-seq data.BMC microbiology · 2022Article
- Infectious origin of Alzheimer's disease: Amyloid beta as a component of brain antimicrobial immunity.PLoS pathogens · 2022Review
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
The disease known as late-onset Alzheimer's disease is a neurodegenerative condition recognized as the single most commonform of senile dementia. The condition is sporadic and has been attributed to neuronal damage and loss, both of which have been linked to the accumulation of protein deposits in the brain. Significant progress has been made over the past two decades regarding our overall understanding of the apparently pathogenic entities that arise in the affected brain, both for early-onset disease, which constitutes approximately 5% of all cases, as well as late-onset disease, which constitutes the remainder of cases. Observable neuropathology includes: neurofibrillary tangles, neuropil threads, neuritic senile plaques and often deposits of amyloid around the cerebrovasculature. Although many studies have provided a relatively detailed knowledge of these putatively pathogenic entities, understanding of the events that initiate and support the biological processes generating them and the subsequent observable neuropathology and neurodegeneration remain limited. This is especially true in the case of late-onset disease. Although early-onset Alzheimer's disease has been shown conclusively to have genetic roots, the detailed etiologic initiation of late-onset disease without such genetic origins has remained elusive. Over the last 15 years, current and ongoing work has implicated infection in the etiology and pathogenesis of late-onset dementia. Infectious agents reported to be associated with disease initiation are various, including several viruses and pathogenic bacterial species. We have reported extensively regarding an association between late-onset disease and infection with the intracellular bacterial pathogen
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Registered trials
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.