SynthesisCNS drugs2020
Targeting Infectious Agents as a Therapeutic Strategy in Alzheimer's Disease.
Synthesis in CNS drugs, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 35 citations in OpenAlex.
- Gut-brain axis in health and brain disease.Chinese medical journal · 2026Review
- Traffic-related air pollution significantly aggravates the detrimental effect of infections on the risk of Alzheimer's disease and other dementias, especially in non-carriers ofFrontiers in dementia · 2025Article
- Are current etiological theories of Alzheimer's disease falsifiable? An epistemological assessment.Frontiers in aging neuroscience · 2025Article
- The role of probiotics, prebiotics, and postbiotics: cellular and molecular pathways activated on glial cells in Alzheimer's disease.Frontiers in neuroscience · 2025Review
- Molecular Mechanisms Linking Osteoarthritis and Alzheimer's Disease: Shared Pathways, Mechanisms and Breakthrough Prospects.International journal of molecular sciences · 2024Review
- Prior infections are associated with smaller hippocampal volume in older women.Frontiers in dementia · 2024Article
- Elevated lipopolysaccharide binding protein in Alzheimer's disease patients withFrontiers in neurology · 2024Article
- A Scoping Review of Alzheimers Disease Hypotheses: An Array of Uni- and Multi-Factorial Theories.Journal of Alzheimer's disease : JAD · 2024Article
- Alleviation of Cognitive Impairment-like Behaviors, Neuroinflammation, Colitis, and Gut Dysbiosis in 5xFAD Transgenic and Aged Mice byNutrients · 2023Article
- ProbioticMicroorganisms · 2023Article
- A glance through the effects of CD4Computational and structural biotechnology journal · 2023Review
- Evidence supportive of a bacterial component in the etiology for Alzheimer's disease and for a temporal-spatial development of a pathogenic microbiome in the brain.Frontiers in cellular and infection microbiology · 2023Article
- Multi-pathogen infections and Alzheimer's disease.Microbial cell factories · 2021Review
- Targeting Impaired Antimicrobial Immunity in the Brain for the Treatment of Alzheimer's Disease.Neuropsychiatric disease and treatment · 2021Review
- Red Cell Distribution Width, Anemia, and Brain Volumetric Outcomes Among Middle-Aged Adults.Journal of Alzheimer's disease : JAD · 2021Article
- Evidence for aggregation-independent, PrPProceedings of the National Academy of Sciences of the United States of America · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 9 institutions in 9 countries.
Funding
Abstract
Alzheimer's disease (AD) is the most prevalent dementia in the world. Its cause(s) are presently largely unknown. The most common explanation for AD, now, is the amyloid cascade hypothesis, which states that the cause of AD is senile plaque formation by the amyloid β peptide, and the formation of neurofibrillary tangles by hyperphosphorylated tau. A second, burgeoning theory by which to explain AD is based on the infection hypothesis. Much experimental and epidemiological data support the involvement of infections in the development of dementia. According to this mechanism, the infection either directly or via microbial virulence factors precedes the formation of amyloid β plaques. The amyloid β peptide, possessing antimicrobial properties, may be beneficial at an early stage of AD, but becomes detrimental with the progression of the disease, concomitantly with alterations to the innate immune system at both the peripheral and central levels. Infection results in neuroinflammation, leading to, and sustained by, systemic inflammation, causing eventual neurodegeneration, and the senescence of the immune cells. The sources of AD-involved microbes are various body microbiome communities from the gut, mouth, nose, and skin. The infection hypothesis of AD opens a vista to new therapeutic approaches, either by treating the infection itself or modulating the immune system, its senescence, or the body's metabolism, either separately, in parallel, or in a multi-step way.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.