Evidence map›Paper›PMID 35922737›Full record

ArticleInflammopharmacology2022

Glimepiride mitigates tauopathy and neuroinflammation in P301S transgenic mice: role of AKT/GSK3β signaling.

Mennatallah O Zaki, S El-Desouky, Doaa A Elsherbiny, Mohamed Salama, Samar S Azab

RetractedOpen access · hybridAbstract readRetracted Publication
In one paragraph

Article in Inflammopharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.0field-weighted citation impact, top 28% 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

6 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
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  3. Review
  4. Review
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  6. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 1 country.

Mennatallah O ZakiDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Horus University, New Damietta, Egypt.
S El-DesoukyMedical Experimental Research Center (MERC), Faculty of Medicine, Mansoura University, Mansoura, Egypt.
Doaa A ElsherbinyDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Ain Shams University, Cairo, 11566, Egypt.
Mohamed SalamaMedical Experimental Research Center (MERC), Faculty of Medicine, Mansoura University, Mansoura, Egypt.
Samar S AzabDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Ain Shams University, Cairo, 11566, Egypt. samar_saad_azab@pharma.asu.edu.eg.ORCID http://orcid.org/0000-0002-0253-8280
Ain Shams University · EGMansoura University · EGDamietta University · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

objectiveTauopathy is a group of neurodegenerative diseases in which the pathogenesis processes are related to tau protein. The imbalances between the activities of kinases and phosphatases of tau protein lead to tau hyperphosphorylation and subsequent neurodegeneration. Numerous studies suggest a strong linkage between type 2 diabetes mellitus (T2D) and neurodegenerative diseases. Therefore, finding a drug with a dual therapeutic activity against T2D and neuroprotective will be a promising idea. Hence, the potential neuroprotective effect of Glimepiride (GPD) against tauopathy was evaluated in the current study.

methodsP301S mice model was employed for tauopathy and C57BL/6 wild type mice (WT) was used as control. Phosphorylated and acetylated tau protein levels was assessed in cortex and hippocampus by western blot. Effect of GPD on tauopathy related enzymes, neuroinflammation, apoptotic markers were evaluated. Furthermore, the neuroprotective effects against anxiety like behavior and motor impairment was analyzed using Parallel rod floor and Open field tests.

resultsGPD significantly ameliorates motor impairment, anxiety like behavior and neurodegeneration in P301S mice. Phosphorylated tau and acetylated tau were significantly decreased in both cortex and hippocampus of P301S mice via decreasing GSK3β, increasing ratio of phosphorylated-AKT to total-AKT, increasing PP2A and normalization of CDK5 levels. Furthermore, GPD treatment also decreased neuroinflammation and apoptosis by reducing NF-kB, TNF-α and caspase 3 levels.

conclusionThe current data suggests that GPD exerts a protective effect against tauopathy, behavioural consequences, neurodegeneration, neuroinflammation and apoptosis. GPD is therefore a promising agent for the treatment of neurodegenerative diseases associated with tauopathy.

Indexed as

Diabetes Mellitus, Type 2Neurodegenerative DiseasesNeuroprotective AgentsTauopathiesAnimalsCaspase 3Disease Models, AnimalGlycogen Synthase Kinase 3 betaMiceMice, Inbred C57BLMice, TransgenicNeuroinflammatory DiseasesNF-kappa BPhosphoric Monoester HydrolasesProto-Oncogene Proteins c-aktSulfonylurea CompoundsCaspase 3glimepirideGlycogen Synthase Kinase 3 betaNeuroprotective AgentsNF-kappa BPhosphoric Monoester HydrolasesProto-Oncogene Proteins c-aktSulfonylurea Compoundstau ProteinsTumor Necrosis Factor-alphaGlimepirideGSK3βNeuroinflammationP301SPP2ATauopathy

Identifiers

PMID35922737
PMCPMC9499917
OpenAlexW4289654007

What Socratic holds

Textmetadata
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.