Evidence map›Paper›PMID 25210802›Full record

ArticleCell death & disease2014

Palmitoylethanolamide controls reactive gliosis and exerts neuroprotective functions in a rat model of Alzheimer's disease.

C Scuderi, C Stecca, M Valenza, P Ratano, M R Bronzuoli, S Bartoli, L Steardo, E Pompili, L Fumagalli, P Campolongo and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 2 pooled it
2.8field-weighted citation impact, top 10% 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

58 citing papers in PubMed, 2 syntheses or guidelines pooled it, 95 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Natural Molecules for Brain Health and Resilience.International journal of molecular sciences · 2026
    Review
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  7. Article
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  9. Article
  10. Chronic palmitoylethanolamide administrationFrontiers in cellular neuroscience · 2025
    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

11 authors at 3 institutions in 2 countries.

C ScuderiDepartment of Physiology and Pharmacology 'Vittorio Erspamer'-SAPIENZA University of Rome, P.le A. Moro, Rome 5-00185, Italy.
C SteccaDepartment of Physiology and Pharmacology 'Vittorio Erspamer'-SAPIENZA University of Rome, P.le A. Moro, Rome 5-00185, Italy.
M ValenzaLaboratory of the Biology of Addictive Diseases-The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA.
P RatanoDepartment of Physiology and Pharmacology 'Vittorio Erspamer'-SAPIENZA University of Rome, P.le A. Moro, Rome 5-00185, Italy.
M R BronzuoliDepartment of Physiology and Pharmacology 'Vittorio Erspamer'-SAPIENZA University of Rome, P.le A. Moro, Rome 5-00185, Italy.
S BartoliDepartment of Physiology and Pharmacology 'Vittorio Erspamer'-SAPIENZA University of Rome, P.le A. Moro, Rome 5-00185, Italy.
L SteardoDepartment of Psychiatry-University of Naples SUN, Largo Madonna delle Grazie, Naples 1-80138, Italy.
E PompiliDepartment of Anatomy, Histology, Forensic Medicine and Orthopedics-SAPIENZA University of Rome, Via A. Borelli 50, Rome 00161, Italy.
L FumagalliDepartment of Anatomy, Histology, Forensic Medicine and Orthopedics-SAPIENZA University of Rome, Via A. Borelli 50, Rome 00161, Italy.
P CampolongoDepartment of Physiology and Pharmacology 'Vittorio Erspamer'-SAPIENZA University of Rome, P.le A. Moro, Rome 5-00185, Italy.
L SteardoDepartment of Physiology and Pharmacology 'Vittorio Erspamer'-SAPIENZA University of Rome, P.le A. Moro, Rome 5-00185, Italy.
Sapienza University of Rome · ITUniversity of Naples Federico II · ITRockefeller University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Given the complex heterogeneity of pathological changes occurring in Alzheimer's disease (AD), any therapeutic effort absolutely requires a multi-targeted approach, because attempts addressing only a single event may result ineffective. Palmitoylethanolamide (PEA), a naturally occurring lipid amide between palmitic acid and ethanolamine, seems to be a compound able to fulfill the criteria of a multi-factorial therapeutic approach. Here, we describe the anti-inflammatory and neuroprotective activities of systemic administration of PEA in adult male rats given intrahippocampal injection of beta amyloid 1-42 (Aβ 1-42). Moreover, to investigate the molecular mechanisms responsible for the effects induced by PEA, we co-administered PEA with the GW6471, an antagonist of peroxisome proliferator-activated receptor-α (PPAR-α). We found that Aβ 1-42 infusion results in severe changes of biochemical markers related to reactive gliosis, amyloidogenesis, and tau protein hyperphosphorylation. Interestingly, PEA was able to restore the Aβ 1-42-induced alterations through PPAR-α involvement. In addition, results from the Morris water maze task highlighted a mild cognitive deficit during the reversal learning phase of the behavioral study. Similarly to the biochemical data, also mnestic deficits were reduced by PEA treatment. These data disclose novel findings about the therapeutic potential of PEA, and suggest novel strategies that hopefully could have the potential not just to alleviate the symptoms but also to modify disease progression.

Indexed as

Alzheimer DiseaseAmidesAnimalsDisease Models, AnimalEthanolaminesGliosisHumansMaleNeuroprotective AgentsPalmitic AcidsPPAR alphaRatsRats, Sprague-DawleyAmidesEthanolaminesNeuroprotective AgentspalmidrolPalmitic AcidsPPAR alpha

Identifiers

PMID25210802
PMCPMC4540191
OpenAlexW1985187905

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.