ReviewFrontiers in cellular neuroscience2016
The Therapeutic Potential of Targeting Substance P/NK-1R Interactions in Inflammatory CNS Disorders.
Review in Frontiers in cellular neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 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
68 citing papers in PubMed, 1 synthesis or guideline pooled it, 120 citations in OpenAlex.
- Clinical Applications of Substance P (Neurokinin-1 Receptor) Antagonist in Canine Medicine.Archives of Razi Institute · 2021Pooled it
- TRPV1‑mediated central sensitisation: Core mechanisms of migraine chronification and novel targeted therapeutic strategies (Review).International journal of molecular medicine · 2026Review
- Substance P and NK-1R in Dengue: A First Serological Investigation.Health science reports · 2026Article
- Multivalent antibody-based conjugates as new tools for tailored modulation of G protein-coupled receptors.British journal of pharmacology · 2026Review
- An attention-demanding hunting paradigm engages the superior colliculus-zona incerta circuit mediating analgesia in male mice.Nature communications · 2026Article
- Mast Cells and Substance P: Neuroinflammatory Loops at the Molecular and Translational Clinical Levels.Biomolecules · 2026Review
- Neuropeptides in the Management of Alzheimer's Disease: From Pathophysiology to Therapeutic Opportunities.International journal of molecular sciences · 2026Review
- Role of Angiotensin-Converting Enzyme in Cognitive Aging: Evidence from Preclinical and Clinical Studies.Frontiers in drug discovery · 2026Article
- Adipose Tissue and Central Nervous System Crosstalk: Roles in Pain and Cognitive Dysfunction.Biomedicines · 2025Review
- Virtual screening of drugs against multiple targets of Alzheimer's disease.Journal of Alzheimer's disease : JAD · 2025Article
- What a pain in the back: etiology, diagnosis and future treatment directions for discogenic low back pain.Bone research · 2025Review
- Substance P Augments Chemokine Production by Staphylococcus aureus Infected Murine Osteoclasts.Inflammation · 2025Article
- Tumor Innervation: From Bystander to Emerging Therapeutic Target for Cancer.International journal of molecular sciences · 2025Review
- Disruption of DNA methylation underpins the neuroinflammation induced by targeted CNS radiotherapy.Brain : a journal of neurology · 2025Article
- The Relationship Between Inflammation and the Development of Cerebral Ischaemia and Hypoxia in Traumatic Brain Injury-A Narrative Review.International journal of molecular sciences · 2025Review
- Tachykinin Receptors and their Antagonists: Unraveling Their Role in Metabolic Disorders and Therapeutic Innovations.Current drug targets · 2025Review
- The Double-Edged Effects of Substance P in the Pathology of Alzheimer's Disease.Aging and disease · 2024Review
- NK1 tachykinin receptor antagonist treatment reduces cerebral edema and intracranial pressure in an ovine model of ischemic stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024Article
- Evaluating the Role of N-Acetyl-L-Tryptophan in the Aβ 1-42-Induced Neuroinflammation and Cognitive Decline in Alzheimer's Disease.Molecular neurobiology · 2024Article
- Molecular Aspects Involved in the Mechanisms ofToxins · 2024Article
8 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The inflammatory responses of resident central nervous system (CNS) cells are now known to play a critical role in the initiation and progression of an array of infectious and sterile neuroinflammatory disorders such as meningitis, encephalitis, Parkinson's disease, Alzheimer's disease and multiple sclerosis (MS). Regulating glial inflammatory responses in a timely manner is therefore critical in preserving normal CNS functions. The neuropeptide substance P is produced at high levels within the CNS and its selective receptor, the neurokinin 1 receptor (NK-1R), is abundantly expressed by neurons and is present on glial cell types including microglia and astrocytes. In addition to its functions as a neurotransmitter in the perception of pain and its essential role in gut motility, this tachykinin is widely recognized to exacerbate inflammation at peripheral sites including the skin, gastrointestinal tract and the lungs. Recently, a number of studies have identified a role for substance P and NK-1R interactions in neuroinflammation and described the ability of this neuropeptide to alter the immune functions of activated microglia and astrocytes. In this review article, we describe the expression of substance P and its receptor by resident CNS cells, and we discuss the ability of this neuropeptide to exacerbate the inflammatory responses of glia and immune cells that are recruited to the brain during neurodegenerative diseases. In addition, we discuss the available data indicating that the NK-1R-mediated augmentation of such responses appears to be detrimental during microbial infection and some sterile neurodegenerative disorders, and propose the repurposed use of NK-1R antagonists, of a type that are currently approved as anti-emetic and anti-anxiolytic agents, as an adjunct therapy to ameliorate the inflammatory CNS damage in these conditions.
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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.