ArticleJournal of neuroinflammation2019
Beneficial effects of curtailing immune susceptibility in an Alzheimer's disease model.
Article in Journal of neuroinflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 39 citations in OpenAlex.
- The spleen-brain axis in Alzheimer's disease and related dementias: Integrating immune and metabolic regulation.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Pharmacokinetic and Pharmacodynamic Evaluation of PZ-2891, an Anti-Alzheimer's Disease Agonist of PANK2.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Dantrolene normalizes heightened CaCell calcium · 2025Article
- Rebalancing Immune Interactions within the Brain-Spleen Axis Mitigates Neuroinflammation in an Aging Mouse Model of Alzheimer's Disease.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
- Microglia either promote or restrain TRAIL-mediated excitotoxicity caused by AβJournal of neuroinflammation · 2024Article
- Prodromic Inflammatory-Oxidative Stress in Peritoneal Leukocytes of Triple-Transgenic Mice for Alzheimer's Disease.International journal of molecular sciences · 2024Article
- Glomerular Hypertrophy and Splenic Red Pulp Degeneration Concurrent with Oxidative Stress in 3xTg-AD Mice Model for Alzheimer's Disease and Its Exacerbation with Sex and Social Isolation.International journal of molecular sciences · 2024Article
- N-acetylneuraminic acid links immune exhaustion and accelerated memory deficit in diet-induced obese Alzheimer's disease mouse model.Nature communications · 2023Article
- Recent Advances in the Development of Nanodelivery Systems Targeting the TRAIL Death Receptor Pathway.Pharmaceutics · 2023Review
- Acupuncture regulates the Th17/Treg balance and improves cognitive deficits in a rat model of vascular dementia.Heliyon · 2023Article
- Neuroinflammation as a mechanism linking hypertension with the increased risk of Alzheimer's disease.Neural regeneration research · 2022Review
- TRAIL-R Deficient Mice Are Protected from Neurotoxic Effects of Amyloid-β.International journal of molecular sciences · 2022Article
- Article
- Differences in Immune-Related Genes Underlie Temporal and Regional Pathological Progression in 3xTg-AD Mice.Cells · 2022Article
- Physiological clearance of Aβ by spleen and splenectomy aggravates Alzheimer-type pathogenesis.Aging cell · 2022Article
- Targeting the miRNA-155/TNFSF10 network restrains inflammatory response in the retina in a mouse model of Alzheimer's disease.Cell death & disease · 2021Article
- Comparative Transcriptome Analysis of the Expression of Antioxidant and Immunity Genes in the Spleen of a Cyanidin 3-O-Glucoside-Treated Alzheimer's Mouse Model.Antioxidants (Basel, Switzerland) · 2021Article
- TRAIL Mediates Neuronal Death in AUD: A Link between Neuroinflammation and Neurodegeneration.International journal of molecular sciences · 2021Article
- Article
- Differential effects of chronic immunosuppression on behavioral, epigenetic, and Alzheimer's disease-associated markers in 3xTg-AD mice.Alzheimer's research & therapy · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCurrently, there are no effective therapeutic options for Alzheimer's disease, the most common, multifactorial form of dementia, characterized by anomalous amyloid accumulation in the brain. Growing evidence points to neuroinflammation as a major promoter of AD. We have previously shown that the proinflammatory cytokine TNFSF10 fuels AD neuroinflammation, and that its immunoneutralization results in improved cognition in the 3xTg-AD mouse.
methodsHere, we hypothesize that inflammatory hallmarks of AD might parallel with central and peripheral immune response dysfunction. To verify such hypothesis, we used a triple transgenic mouse model of AD. 3xTg-AD mice were treated for 12 months with an anti-TNFSF10 antibody, and thereafter immune/inflammatory markers including COX2, iNOS, IL-1β and TNF-α, CD3, GITR, and FoxP3 (markers of regulatory T cells) were measured in the spleen as well as in the hippocampus.
resultsSpleens displayed accumulation of amyloid-β
conclusionsWe suggest that neuroinflammation in the brain of 3xTg-AD mice triggered by TNFSF10 might result in a more general overshooting of the immune response. Treatment with an anti-TNFSF10 antibody blunted inflammatory processes both in the spleen and hippocampus. These data confirm the detrimental role of TNFSF10 in neurodegeneration, and corroborate the hypothesis of the anti-TNFSF10 strategy as a potential treatment to improve outcomes in AD.
Indexed as
Identifiers
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.