Evidence map›Paper›PMID 32033363›Full record

ArticleJournal of clinical medicine2020

Chronic Oral Palmitoylethanolamide Administration Rescues Cognitive Deficit and Reduces Neuroinflammation, Oxidative Stress, and Glutamate Levels in A Transgenic Murine Model of Alzheimer's Disease.

Sarah Beggiato, Maria Cristina Tomasini, Tommaso Cassano, Luca Ferraro

Open access · goldAbstract read
In one paragraph

Article in Journal of clinical medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 2 pooled it
3.3field-weighted citation impact, top 7% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

28 citing papers in PubMed, 2 syntheses or guidelines pooled it, 35 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Palmitoylethanolamide in Human and Animal Obesity.Molecules (Basel, Switzerland) · 2026
    Review
  4. Review
  5. Natural Molecules for Brain Health and Resilience.International journal of molecular sciences · 2026
    Review
  6. Palmitoylethanolamide (PEA) in the treatment of restless legs syndrome: Rationale and case report.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Sarah BeggiatoDepartment of Life Sciences and Biotechnology, University of Ferrara, 44121 Ferrara, Italy.
Maria Cristina TomasiniDepartment of Life Sciences and Biotechnology, University of Ferrara, 44121 Ferrara, Italy.
Tommaso CassanoDepartment of Clinical and Experimental Medicine, University of Foggia, 71122 Foggia, Italy.
Luca FerraroDepartment of Life Sciences and Biotechnology, University of Ferrara, 44121 Ferrara, Italy.
University of Ferrara · ITUniversity of Foggia · IT

Funding

ALTERNATIVE PATHWAYS OF T CELL ACTIVATIONK08AR002017 · NIAMS · VANDERBILT UNIVERSITY · PI BYRD, VICTOR M · 1998 to 2002
$348k
ANDROGEN REGULATION OF HUMAN SEBACEOUS GLANDSK08AR002018 · NIAMS · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI THIBOUTOT, DIANE M. · 1997 to 2001
$225k
Alzheimer's Drug Discovery Foundation 20151001University of Ferrara FAR2017University of Ferrara FAR2018
6 · The paper itself

Abstract

N-palmitoylethanolamide (PEA) is a lipid mediator belonging to the class of the N-acylethanolamine. Products containing PEA, also in ultramicronized formulation (um-PEA), are already licensed for use in humans for its analgesic and anti-inflammatory properties, and demonstrated high safety and tolerability. Preclinical studies indicate that PEA, especially in the ultramicronized form, could be a potential therapeutic agent for Alzheimer's disease (AD). In this study, we evaluated the neuroprotective and antioxidant effects of chronic (three months) um-PEA administration in an animal model of AD (3×Tg-AD mice). For translation purposes, the compound has been orally administered. Cognitive performance as well as biochemical markers [(interleukin-16 (IL-16) and tumor necrosis factor- (TNF-)] levels, reactive oxygen species (ROS) production, synaptophysin and glutamate levels) have been evaluated at the end of um-PEA treatment. The results indicate that orally administered um-PEA was adsorbed and distributed in the mice brain. The chronic treatment with um-PEA (100 mg/kg/day for three months) rescued cognitive deficit, restrained neuroinflammation and oxidative stress, and reduced the increase in hippocampal glutamate levels observed in 3×Tg-AD mice. Overall, these data reinforce the concept that um-PEA exerts beneficial effects in 3×Tg-AD mice. The fact that PEA is already licensed for the use in humans strongly supports its rapid translation in clinical practice.

Indexed as

Alzheimer’s diseasecognitive dysfunctionsextracellular glutamate levelshippocampusreactive oxygen speciessynaptophysin

Identifiers

PMID32033363
PMCPMC7074257
OpenAlexW3005268186

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.