ReviewFrontiers in pharmacology2019
Neuroinflammation as a Common Feature of Neurodegenerative Disorders.
Review in Frontiers in pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 428 papers, 5 of them syntheses that pooled it.
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Who cites it
428 citing papers in PubMed, 5 syntheses or guidelines pooled it.
- Meta-analysis of Cognitive Function Following Non-severe SARS-CoV-2 Infection.Neuropsychology review · 2025Pooled it
- Apigenin and inflammation in the brain: can apigenin inhibit neuroinflammation in preclinical models?Inflammopharmacology · 2024Pooled it
- Pooled it
- Neurodegenerative Disease Associated Pathways in the Brains of Triple Transgenic Alzheimer's Model Mice Are Reversed Following Two Weeks of Peripheral Administration of Fasudil.International journal of molecular sciences · 2023Pooled it
- GFAP as a Potential Biomarker for Alzheimer's Disease: A Systematic Review and Meta-Analysis.Cells · 2023Pooled it
- Trial
- Phytochemical Profile, Antioxidant Activity, and Anti-Neuroinflammatory Effects of a Novel Dry Extract of Libidibia ferrea in Microglial Cells.Chemistry & biodiversity · 2026Article
- Regulation of NLRP3 inflammasome signaling in Alzheimer's disease: emerging neuroprotective role of phytochemicals.Inflammopharmacology · 2026Review
- Review
- Single nuclear RNA sequencing shows altered microglial and astrocytic functions in post-mortem Parkinson's disease tissue.BMC genomic data · 2026Article
- Regional mapping of CSF1R-positive microglia in neurodegenerative diseases and progressive MS, with exploratory presynaptic marker analyses.Journal of neuroinflammation · 2026Article
- Review
- Exploration of the genetic neuroinflammatory environment in the human midcingulate cortex in Huntington's disease.Communications medicine · 2026Article
- Feasibility of multimodal metabolic analysis for detecting early changes in acute neuroinflammation.Journal of neuroinflammation · 2026Article
- Multi-Target-Directed Ligands (MTDLs) as Potential Therapeutic Candidates Targeting Multiple Pathogenic Factor of Alzheimer's Disease.CNS neuroscience & therapeutics · 2026Review
- The essential role of hydrogen gas recycling by gut microbes in reducing deuterium load in host mitochondria: is trimethylamine oxide a deuterium sensor?Metabolomics : Official journal of the Metabolomic Society · 2026Review
- Autophagy-Neuroinflammation Axis in Neurodegenerative Diseases: Mechanisms and Therapeutic Potential.Cells · 2026Review
- Naftidrofuryl Exerts Neuroprotective Effects in a Rotenone-Induced Rat Model of Parkinson's Disease Through Modulation of PINK1/Parkin and ER Stress Pathways.Neuromolecular medicine · 2026Article
- Therapeutic potential of sulforaphane in neurodegenerative diseases: mechanistic Insights into Nrf2, NF-κB, TrkB, SIRT1, MAPK, and JAK/STAT signalling pathways.Molecular biology reports · 2026Review
- Transcriptome analysis of the prefrontal cortex identifies inflammatory genes associated with cognitive impairment in a model of multiple sclerosis.Cell death discovery · 2026Article
368 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neurodegenerative diseases share the fact that they derive from altered proteins that undergo an unfolding process followed by formation of β-structures and a pathological tendency to self-aggregate in neuronal cells. This is a characteristic of tau protein in Alzheimer's disease and several tauopathies associated with tau unfolding, α-synuclein in Parkinson's disease, and huntingtin in Huntington disease. Usually, the self-aggregation products are toxic to these cells, and toxicity spreads all over different brain areas. We have postulated that these protein unfolding events are the molecular alterations that trigger several neurodegenerative disorders. Most interestingly, these events occur as a result of neuroinflammatory cascades involving alterations in the cross-talks between glial cells and neurons as a consequence of the activation of microglia and astrocytes. The model we have hypothesized for Alzheimer's disease involves damage signals that promote glial activation, followed by nuclear factor NF-kβ activation, synthesis, and release of proinflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-1, IL-6, and IL-12 that affect neuronal receptors with an overactivation of protein kinases. These patterns of pathological events can be applied to several neurodegenerative disorders. In this context, the involvement of innate immunity seems to be a major paradigm in the pathogenesis of these diseases. This is an important element for the search for potential therapeutic approaches for all these brain disorders.
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