ReviewJournal of neuroinflammation2015
Rodent models of neuroinflammation for Alzheimer's disease.
Review in Journal of neuroinflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers, 1 of them a synthesis that pooled it.
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Who cites it
116 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Effect of berberine on cognitive function and β-amyloid precursor protein in Alzheimer's disease models: a systematic review and meta-analysis.Frontiers in pharmacology · 2023Pooled it
- Microglial synaptic pruning in early Alzheimer's disease: emerging roles of the IL-1β-NLRP3 axis.Inflammopharmacology · 2026Review
- Phytohemagglutinin: A Tool for Inducing Neuroinflammation Mediated In Vitro and In Vivo Modeling of Alzheimer's Disease Pathology.Cell biochemistry and function · 2026Article
- Longitudinal multimodal assessment of neuropathy in a porcine neuritis model.Journal of neuroscience methods · 2026Article
- Beyond diabetes and obesity: GLP-1 receptor agonists in disrupting the vicious cycle of metabolic dysfunction and neuroinflammation.Diabetes, obesity & metabolism · 2026Review
- The 3xTg-AD Mouse Model: A Comprehensive Tool for Understanding Alzheimer's Disease.Cellular and molecular neurobiology · 2026Review
- Neuroprotective mechanism of hydrogen sulfide in okadaic acid-induced alzheimer-like pathology.GeroScience · 2026Article
- Experimental Models and Translational Strategies in Neuroprotective Drug Development with Emphasis on Alzheimer's Disease.Molecules (Basel, Switzerland) · 2026Review
- Unraveling the oral microbiome's role in Alzheimer's disease: From pathophysiology to therapeutic potential.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- Noninvasive Brain Stimulation Protects Cognitive Impairment in i.c.v. STZ-Injected Rats: Role of Adult Neurogenesis.The European journal of neuroscience · 2025Article
- Exploring Gastrodin Against Aging-Related Genes in Alzheimer's Disease by Integrated Bioinformatics Analysis and Machine Learning.International journal of molecular sciences · 2025Article
- Microbiota-gut-brain axis in neurodegenerative diseases: molecular mechanisms and therapeutic targets.Molecular biomedicine · 2025Review
- Navigation Between Alzheimer's Disease (AD) and Its Various Pathophysiological Trajectories: The Pathogenic Link to Neuroimmunology-Genetics and Neuroinflammation.International journal of molecular sciences · 2025Review
- GDNF overexpression in astrocytes enhances branching and partially preserves hippocampal function in an Alzheimer's rat model.Scientific reports · 2025Article
- The neurobiological foundation of effective repetitive transcranial magnetic brain stimulation in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- A Novel Missense Variant in SORBS2 Is Causative With Familial Alzheimer's Disease.CNS neuroscience & therapeutics · 2025Article
- Aryl hydrocarbon receptor deficiency enhances astrocyte sensitivity to LPS-induced inflammation.Frontiers in cellular neuroscience · 2025Article
- Primary cortical cell tri-culture to study effects of amyloid-β on microglia function and neuroinflammatory response.Journal of Alzheimer's disease : JAD · 2024Article
- Establishment and optimization of a novel mouse model of hyperuricemic nephropathy.Renal failure · 2024Article
- Locomotor and gait changes in the LPS model of neuroinflammation are correlated with inflammatory cytokines in blood and brain.Journal of inflammation (London, England) · 2024Article
56 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease remains incurable, and the failures of current disease-modifying strategies for Alzheimer's disease could be attributed to a lack of in vivo models that recapitulate the underlying etiology of late-onset Alzheimer's disease. The etiology of late-onset Alzheimer's disease is not based on mutations related to amyloid-β (Aβ) or tau production which are currently the basis of in vivo models of Alzheimer's disease. It has recently been suggested that mechanisms like chronic neuroinflammation may occur prior to amyloid-β and tau pathologies in late-onset Alzheimer's disease. The aim of this study is to analyze the characteristics of rodent models of neuroinflammation in late-onset Alzheimer's disease. Our search criteria were based on characteristics of an idealistic disease model that should recapitulate causes, symptoms, and lesions in a chronological order similar to the actual disease. Therefore, a model based on the inflammation hypothesis of late-onset Alzheimer's disease should include the following features: (i) primary chronic neuroinflammation, (ii) manifestations of memory and cognitive impairment, and (iii) late development of tau and Aβ pathologies. The following models fit the pre-defined criteria: lipopolysaccharide- and PolyI:C-induced models of immune challenge; streptozotocin-, okadaic acid-, and colchicine neurotoxin-induced neuroinflammation models, as well as interleukin-1β, anti-nerve growth factor and p25 transgenic models. Among these models, streptozotocin, PolyI:C-induced, and p25 neuroinflammation models are compatible with the inflammation hypothesis of Alzheimer's disease.
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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.