ReviewCells2025
Modulating Neuroinflammation as a Prospective Therapeutic Target in Alzheimer's Disease.
Review in Cells, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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
19 citing papers in PubMed, 1 synthesis or guideline pooled it.
- From Tradition to Innovation: Acupuncture Therapies Targeting Ferroptosis in Neurological Disorders.Brain and behavior · 2025Pooled it
- Neuroinflammatory and molecular pathways in Alzheimer's disease: mechanistic crosstalk and emerging therapeutic opportunities.Inflammopharmacology · 2026Review
- AgeViva Modulates Inflammatory Responses, Autophagy, and Mitochondrial Homeostasis in BV-2 Cells andMetabolites · 2026Article
- Magnoflorine and its structural diversity: mechanisms, and drug discovery opportunities a review.Molecular diversity · 2026Review
- Rodent Models of Alzheimer's Disease: Bridging the Translational Gap Through Systems-Level Integration.Biomedicines · 2026Review
- Repurposing apremilast for alzheimer's disease: multitarget modulation of cAMP‑PI3K/Akt-GSK‑3β and NF‑κB signaling.Metabolic brain disease · 2026Review
- The Interplay Between Immunometabolism and Neuroinflammation in Alzheimer's Disease.Biomolecules · 2026Review
- Delivery of miR-25802 via Small Vesicles Protects Against Mitochondrial Injury, Oxidative Stress, and Neuroinflammation in Alzheimer's Disease.Molecular neurobiology · 2026Article
- New Oligophenalenone Dimers fromMolecules (Basel, Switzerland) · 2026Article
- Store-operated calcium entry drives alcohol-exacerbated neuroinflammation in retinal degeneration.Cell death discovery · 2026Article
- Microglia-Neuron Crosstalk: An Intimate Molecular Conversation in Neurodegeneration.International journal of molecular sciences · 2026Review
- The 3xTg-AD Mouse Model: A Comprehensive Tool for Understanding Alzheimer's Disease.Cellular and molecular neurobiology · 2026Review
- Untargeted plasma metabolomics in canine cognitive dysfunction: the naturally occurring Alzheimer's disease analog in dogs.Frontiers in neuroscience · 2026Article
- Targeting Microglial Activation to Modulate Neuroinflammation in Alzheimer's Disease.Neuromolecular medicine · 2025Review
- NDR2 Kinase Regulates Microglial Metabolic Adaptation and Inflammatory Response: Critical Role in Glucose-Dependent Functional Plasticity.International journal of molecular sciences · 2025Article
- Beyond amyloid: nanobody-mediated neuroinflammatory therapy for Alzheimer's disease.Translational neurodegeneration · 2025Review
- Article
- Therapeutic Potential of a Gadolinium Chelate Complex Conjugated with Vanillic Acid for Alzheimer's Disease.ACS pharmacology & translational science · 2025Article
- The Inflammatory Nexus: Unraveling Shared Pathways and Promising Treatments in Alzheimer's Disease and Schizophrenia.International journal of molecular sciences · 2025Review
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.
Funding
Abstract
The recent approval of lecanemab highlights that the amyloid beta (Aβ) protein is an important pathological target in Alzheimer's disease (AD) and further emphasizes the significance of neuroinflammatory pathways in regulating Aβ accumulation. Indeed, Aβ accumulation triggers microglia activation, which are key mediators in neuroinflammation. The inflammatory responses in this process can lead to neuronal damage and functional decline. Microglia secrete proinflammatory cytokines that accelerate neuronal death and release anti-inflammatory cytokines and growth factors contributing to neuronal recovery and protection. Thus, microglia play a dual role in neurodegeneration and neuroprotection, complicating their function in AD. Therefore, elucidating the complex interactions between Aβ protein, microglia, and neuroinflammation is essential for developing new strategies for treating AD. This review investigates the receptors and pathways involved in activating microglia and aims to enhance understanding of how these processes impact neuroinflammation in AD, as well as how they can be regulated. This review also analyzed studies reported in the existing literature and ongoing clinical trials. Overall, these studies will contribute to understanding the regulatory mechanisms of neuroinflammation and developing new therapies that can slow the pathological progression of 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.