ArticleMediators of inflammation2013
Palmitoylethanolamide is a disease-modifying agent in peripheral neuropathy: pain relief and neuroprotection share a PPAR-alpha-mediated mechanism.
Article in Mediators of inflammation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 72 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
72 citing papers in PubMed, 1 synthesis or guideline pooled it, 134 citations in OpenAlex.
- Palmitoylethanolamide: A Nutritional Approach to Keep Neuroinflammation within Physiological Boundaries-A Systematic Review.International journal of molecular sciences · 2020Pooled it
- Trial
- Efficacy of ultramicronized palmitoylethanolamide in burning mouth syndrome-affected patients: a preliminary randomized double-blind controlled trial.Clinical oral investigations · 2019Trial
- Micronized Palmitoylethanolamide: A Post Hoc Analysis of a Controlled Study in Patients with Low Back Pain - Sciatica.CNS & neurological disorders drug targets · 2019Trial
- Palmitoylethanolamide in Human and Animal Obesity.Molecules (Basel, Switzerland) · 2026Review
- Palmitoylethanolamide (PEA) regulates cell cycle progression and promotes an anti-inflammatory transcriptomic signature in C2C12 skeletal muscle cells.Physiological reports · 2026Article
- Correction to "Palmitoylethanolamide Is a Disease-Modifying Agent in Peripheral Neuropathy: Pain Relief and Neuroprotection Share a PPAR-Alpha-Mediated Mechanism".Mediators of inflammation · 2026Article
- Palmitoylethanolamide: A Multifunctional Molecule for Neuroprotection, Chronic Pain, and Immune Modulation.Biomedicines · 2025Article
- Pain in polycystic ovary syndrome: a comprehensive bedside to bench perspective on an underrecognized symptom.Frontiers in pharmacology · 2025Review
- Treatment of Migraine With Phytocannabinoids, the Involvement of Endocannabinoids in Migraine, and Potential Mechanisms of Action.Pain research & management · 2025Review
- Article
- Palmitoylethanolamide, an endogenous fatty acid amide, and its pleiotropic health benefits: A narrative review.Journal of biomedical research · 2024Article
- Ultramicronized Palmitoylethanolamide in the Management of Neuropathic Pain Related to Chronic Inflammatory Demyelinating Polyneuropathy: A Proof-of-Concept Study.Journal of clinical medicine · 2024Article
- Novel drug treatments for pain in advanced cancer and serious illness: a focus on neuropathic pain and chemotherapy-induced peripheral neuropathy.Palliative care and social practice · 2024Review
- UltramicronizedCurrent neuropharmacology · 2024Article
- Advances in diagnosis and management of distal sensory polyneuropathies.Journal of neurology, neurosurgery, and psychiatry · 2023Review
- UltramicronizedBiomolecules · 2023Article
- Distribution of an analgesic palmitoylethanolamide and other N-acylethanolamines in human placental membranes.PloS one · 2023Article
- Ultrasonic visualization technique for anatomical and functional analyses of the sciatic nerve in rats.Frontiers in neuroscience · 2023Article
- Inhibition of triple negative breast cancer-associated inflammation and progression by N- acylethanolamine acid amide hydrolase (NAAA).Scientific reports · 2022Article
12 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuropathic syndromes which are evoked by lesions to the peripheral or central nervous system are extremely difficult to treat, and available drugs rarely joint an antihyperalgesic with a neurorestorative effect. N-Palmitoylethanolamine (PEA) exerts antinociceptive effects in several animal models and inhibits peripheral inflammation in rodents. Aimed to evaluate the antineuropathic properties of PEA, a damage of the sciatic nerve was induced in mice by chronic constriction injury (CCI) and a subcutaneous daily treatment with 30 mg kg(-1) PEA was performed. On the day 14, PEA prevented pain threshold alterations. Histological studies highlighted that CCI induced oedema and an important infiltrate of CD86 positive cells in the sciatic nerve. Moreover, osmicated preparations revealed a decrease in axon diameter and myelin thickness. Repeated treatments with PEA reduced the presence of oedema and macrophage infiltrate, and a significant higher myelin sheath, axonal diameter, and a number of fibers were observable. In PPAR- α null mice PEA treatment failed to induce pain relief as well as to rescue the peripheral nerve from inflammation and structural derangement. These results strongly suggest that PEA, via a PPAR- α -mediated mechanism, can directly intervene in the nervous tissue alterations responsible for pain, starting to prevent macrophage infiltration.
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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.