Evidence map›Paper›PMID 37458952›Full record

ArticleInflammopharmacology2023

Cognitive enhancing effects of pazopanib in D‑galactose/ovariectomized Alzheimer's rat model: insights into the role of RIPK1/RIPK3/MLKL necroptosis signaling pathway.

Rasha Abdelhady, Nancy S Younis, Omaima Ali, Samah Shehata, Rabab H Sayed, Rania I Nadeem

Open access · hybridAbstract read
In one paragraph

Article in Inflammopharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
5.6field-weighted citation impact, top 5% 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

11 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Non-canonical cell death in neurodegeneration: emerging mechanisms and therapeutic Frontiers.Apoptosis : an international journal on programmed cell death · 2026
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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

6 authors at 5 institutions in 2 countries.

Rasha AbdelhadyDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Fayoum University, Fayoum, Egypt.
Nancy S YounisDepartment of Pharmaceutical Science, Faculty of Clinical Pharmacy, King Faisal University, Al Hofuf 31982, Al-Ahsa, Saudi Arabia.
Omaima AliDepartment of Biochemistry, Faculty of Pharmacy, Sinai University-Kantara Branch, Ismailia, 41636, Egypt.
Samah ShehataDepartment of Biochemistry, Faculty of Pharmacy, Fayoum University, Fayoum, Egypt.
Rabab H SayedDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Kasr El-Aini Street, Cairo, Egypt.
Rania I NadeemDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Heliopolis University, Cairo, P.N. 11785, Egypt. rania.ibrahim@hu.edu.eg.ORCID http://orcid.org/0000-0002-4619-685X
Fayoum University · EGCairo University · EGHeliopolis University · EGKing Faisal University · SASinai University · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Necroptosis, a programmed form of necrotic cell death carried out by receptor-interacting serine/threonine protein kinase 1 (RIPK1) and RIPK3, has been found to be implicated in the pathogenesis of Alzheimer's disease (AD). An FDA-approved anti-cancer drug, pazopanib, is reported to possess potent inhibitory effect against necroptosis via interfering with RIPK1. So far, there are no existing data on the influence of pazopanib on necroptotic pathway in AD. Thus, this study was designed to explore the impact of pazopanib on cognitive impairment provoked by ovariectomy (OVX) together with D-galactose (D-Gal) administration in rats and to scrutinize the putative signaling pathways underlying pazopanib-induced effects. Animals were allocated into four groups; the first and second groups were exposed to sham operation and administered normal saline and pazopanib (5 mg/kg/day, i.p.), respectively, for 6 weeks, while the third and fourth groups underwent OVX then were injected with D-Gal (150 mg/kg/day, i.p.); concomitantly with pazopanib in the fourth group for 6 weeks. Pazopanib ameliorated cognitive deficits as manifested by improved performance in the Morris water maze besides reversing the histological abnormalities. Pazopanib produced a significant decline in p-Tau and amyloid beta (Aβ) plaques. The neuroprotective effect of pazopanib was revealed by hampering neuroinflammation, mitigating neuronal death and suppressing RIPK1/RIPK3/MLKL necroptosis signaling pathway. Accordingly, hindering neuroinflammation and the necroptotic RIPK1/RIPK3/MLKL pathway could contribute to the neuroprotective effect of pazopanib in D-Gal/OVX rat model. Therefore, this study reveals pazopanib as a valuable therapeutic agent in AD that warrants future inspection to provide further data regarding its neuroprotective effect.

Indexed as

Alzheimer DiseaseNeuroprotective AgentsAmyloid beta-PeptidesAnimalsApoptosisCognitionFemaleGalactoseIndazolesNecroptosisNeuroinflammatory DiseasesProtein KinasesPyrimidinesRatsSignal TransductionSulfonamidesAmyloid beta-PeptidesGalactoseIndazolesMLKL protein, ratNeuroprotective AgentspazopanibProtein KinasesPyrimidinesSulfonamidesAlzheimer’s diseaseD‑galactoseMLKL signalingNecroptosisOvariectomizedPazopanibRIPK1RIPK3

Identifiers

PMID37458952
PMCPMC10518286
OpenAlexW4384559479

What Socratic holds

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LicenceCC BY
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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 Socratic graph.