ReviewCurrent neuropharmacology2022
Neuroinflammatory Signaling in the Pathogenesis of Alzheimer's Disease.
Review in Current neuropharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
What it found
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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.
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Who cites it
42 citing papers in PubMed, 68 citations in OpenAlex.
- Dysregulation of neuronal androgen receptor signaling by divergent collaborative transcription factors in Alzheimer's disease.iScience · 2026Article
- Tuberostemonine ameliorates Alzheimer's disease pathology by suppression of the p38 MAPK signaling pathway.iScience · 2026Article
- Therapeutic mechanisms of umbilical cord mesenchymal stem cell-derived exosomes in ischemic stroke: A transcriptomic and metabolomic study.Neural regeneration research · 2026Article
- The Interplay Between Immunometabolism and Neuroinflammation in Alzheimer's Disease.Biomolecules · 2026Review
- Unknotting the Role of circRNAs and IGF2BP3 in Alzheimer's Disease.Cellular and molecular neurobiology · 2026Review
- Self-Assembled Rg3/Naringenin Nanoparticles for Targeted Brain Delivery: A Promising Therapeutic Approach for Early Alzheimer's Disease.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Peptide-Based Therapeutics for Alzheimer's Disease: Medicinal Chemistry, AI-Guided Computational Design, and Blood-Brain Barrier Delivery.Drug design, development and therapy · 2026Review
- Exploring neuroprotective effects of Chuanzhitongluo capsule on an alzheimer's disease rat model.Metabolic brain disease · 2025Article
- Tailoring MAPK Pathways: New Therapeutic Avenues for Treating Alzheimer's Disease.Molecular neurobiology · 2025Review
- Probiotic effects on cognitive performance, hippocampal oxidative stress, and structural damage induced by icv STZ in Alzheimer-like rat model.Brain structure & function · 2025Article
- Potassium homeostasis during disease progression of Alzheimer's disease.The Journal of physiology · 2025Article
- Unmasking a Paradox: Roles of the PD-1/PD-L1 Axis in Alzheimer's Disease-Associated Neuroinflammation.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Review
- Dysregulated interleukin networks drive immune heterogeneity in Alzheimer's disease: an immunogenomic approach to subgroup classification and predictive modeling.BMC neurology · 2025Article
- Follicle-stimulating hormone: More than a marker for menopause: FSH as a frontier for women's mental health.Psychiatry research · 2025Review
- 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
- Article
- The potential link between the development of Alzheimer's disease and osteoporosis.Biogerontology · 2025Review
- Microglial Modulation in Alzheimer's Disease: Central Players in Neuroinflammation and Pathogenesis.Current Alzheimer research · 2025Review
- Dexmedetomidine ameliorates cognitive and affective deficits by modulating neuroinflammation and neurogenesis in an Alzheimer's disease mouse model.Frontiers in aging neuroscience · 2025Article
- Integrative bioinformatics and machine learning identify iron metabolism genes MAP4, GPT, and HIRIP3 as diagnostic biomarkers and therapeutic targets in Alzheimer's disease.Frontiers in cellular neuroscience · 2025Article
Corrections and comments
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Authors and funding
11 authors at 10 institutions in 6 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is a chronic neurodegenerative disease characterized by the formation of intracellular neurofibrillary tangles (NFTs) and extracellular amyloid plaques. Growing evidence has suggested that AD pathogenesis is not only limited to the neuronal compartment but also strongly interacts with immunological processes in the brain. On the other hand, aggregated and misfolded proteins can bind with pattern recognition receptors located on astroglia and microglia and can, in turn, induce an innate immune response, characterized by the release of inflammatory mediators, ultimately playing a role in both the severity and the progression of the disease. It has been reported by genome-wide analysis that several genes which elevate the risk for sporadic AD encode for factors controlling the inflammatory response and glial clearance of misfolded proteins. Obesity and systemic inflammation are examples of external factors which may interfere with the immunological mechanisms of the brain and can induce disease progression. In this review, we discussed the mechanisms and essential role of inflammatory signaling pathways in AD pathogenesis. Indeed, interfering with immune processes and modulation of risk factors may lead to future therapeutic or preventive AD approaches.
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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.