ReviewMolecular neurodegeneration2024
The endotoxin hypothesis of Alzheimer's disease.
Review in Molecular neurodegeneration, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 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
79 citing papers in PubMed, 96 citations in OpenAlex.
- From Dysbiosis to Blood-Brain Barrier Disruption: The Metabolite-Mediated Gut-Brain Axis in Alzheimer's Disease.Molecular neurobiology · 2026Review
- Structure-Guided Optimization of PDE9A Inhibitors Tackling Neuroinflammation: A Combined Computational and In Vitro Study.ChemMedChem · 2026Article
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- Neuroinflammation in Alzheimer's and Parkinson's diseases: pathogenic mechanisms and therapeutic strategies.Translational neurodegeneration · 2026Review
- Silymarin attenuates senescence-exacerbated amyloidogenesis, neuroinflammation, and oxidative stress in lipopolysaccharide-induced memory impairment in aging mice.Biogerontology · 2026Article
- LPS-Induced Neuroinflammation in Neurodegenerative Diseases: A Double-Edged Sword?Molecular neurobiology · 2026Review
- From Tradition to Translation: A Critical Appraisal ofInternational journal of molecular sciences · 2026Review
- Geranylgeraniol promotes osteoblast differentiation and inhibits osteoclastogenesis through MAPK and nuclear receptor signaling.The Journal of biological chemistry · 2026Article
- The complex of gut microbial metabolites and sex hormones in Alzheimer's disease.Seminars in immunopathology · 2026Review
- Regulator of G protein signaling 10: a critical regulator of chronic systemic inflammation in parkinson's disease.Journal of neuroinflammation · 2026Review
- O-GlcNAcylation reprograms microglial inflammatory states and attenuates Alzheimer's disease pathology.Cell death & disease · 2026Article
- Sex-dependent interferon signaling contributes to female-biased vulnerability in Alzheimer's disease.Journal of neuroinflammation · 2026Article
- Review
- 16S rRNA analysis of proximal dental plaque bacteria reveals that daily use of commercialized disposable dental floss ItoyojiBMC oral health · 2026Article
- Targeting the Gut-Brain-Ferroptosis Axis: Molecular Mechanisms and Therapeutic Potential in Alzheimer's Disease and Epilepsy.Journal of molecular neuroscience : MN · 2026Review
- Unmasking the hidden catalyst: How infections trigger Alzheimer's disease.Journal of Alzheimer's disease : JAD · 2026Review
- Effects of Lipopolysaccharide Challenge on Growth Performance and Immune Function of Yellow-Feathered Broilers.Animals : an open access journal from MDPI · 2026Article
- A 3D gut-brain-vascular platform for bidirectional crosstalk in gut-neuropathogenesis.Nature communications · 2026Article
- Gut Dysbiosis and Microbiota-Derived Metabolites in Neurodegenerative Diseases: Molecular and Biochemical Mechanisms Along the Gut-Brain Axis.Molecules (Basel, Switzerland) · 2026Review
19 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
Lipopolysaccharide (LPS) constitutes much of the surface of Gram-negative bacteria, and if LPS enters the human body or brain can induce inflammation and act as an endotoxin. We outline the hypothesis here that LPS may contribute to the pathophysiology of Alzheimer's disease (AD) via peripheral infections or gut dysfunction elevating LPS levels in blood and brain, which promotes: amyloid pathology, tau pathology and microglial activation, contributing to the neurodegeneration of AD. The evidence supporting this hypothesis includes: i) blood and brain levels of LPS are elevated in AD patients, ii) AD risk factors increase LPS levels or response, iii) LPS induces Aβ expression, aggregation, inflammation and neurotoxicity, iv) LPS induces TAU phosphorylation, aggregation and spreading, v) LPS induces microglial priming, activation and neurotoxicity, and vi) blood LPS induces loss of synapses, neurons and memory in AD mouse models, and cognitive dysfunction in humans. However, to test the hypothesis, it is necessary to test whether reducing blood LPS reduces AD risk or progression. If the LPS endotoxin hypothesis is correct, then treatments might include: reducing infections, changing gut microbiome, reducing leaky gut, decreasing blood LPS, or blocking LPS response.
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What OpenQuestion 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 OpenQuestion graph.