Evidence map›Paper›PMID 31728850›Full record

ArticleNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2020

Vildagliptin Attenuates Huntington's Disease through Activation of GLP-1 Receptor/PI3K/Akt/BDNF Pathway in 3-Nitropropionic Acid Rat Model.

Noha H Sayed, Nevine Fathy, Mona A Kortam, Mostafa A Rabie, Ahmed F Mohamed, Ahmed S Kamel

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2020. 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 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
8.1field-weighted citation impact, top 2% 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

61 citing papers in PubMed, 122 citations in OpenAlex.

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1 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Noha H SayedDepartment of Biochemistry, Faculty of Pharmacy, Cairo University, Governorate, Giza, Egypt.
Nevine FathyDepartment of Biochemistry, Faculty of Pharmacy, Cairo University, Governorate, Giza, Egypt. nevine.abdallah@pharma.cu.edu.eg.ORCID http://orcid.org/0000-0002-0033-7215
Mona A KortamDepartment of Biochemistry, Faculty of Pharmacy, Cairo University, Governorate, Giza, Egypt.
Mostafa A RabieDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Governorate, Giza, Egypt.
Ahmed F MohamedDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Governorate, Giza, Egypt.
Ahmed S KamelDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Governorate, Giza, Egypt.
Cairo University · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vildagliptin (Vilda), a dipeptidyl peptidase-4 (DPP-4) inhibitor, has been highlighted as a promising therapeutic agent for neurodegenerative diseases as Alzheimer's and Parkinson's diseases. Vilda's effect is mostly linked to PI3K/Akt signaling in CNS. Moreover, PI3K/Akt activation reportedly enhanced survival and dampened progression of Huntington's disease (HD). However, Vilda's role in HD is yet to be elucidated. Thus, the aim of the study is to uncover the potentiality of Vilda in HD and unfold its link with PI3K/Akt pathway in 3-nitropropionic acid (3NP) rat model. Rats were randomly assigned into 4 groups; group 1 received saline, whereas, groups 2, 3 and 4 received 3NP (10 mg/kg/day; i.p.) for 14 days, concomitantly with Vilda (5 mg/kg/day; p.o.) in groups 3 and 4, and wortmannin (WM), a PI3K inhibitor, (15 μg/kg/day; i.v.) in group 4. Vilda improved cognitive and motor perturbations induced by 3NP, as confirmed by striatal histopathological specimens and immunohistochemical examination of GFAP. The molecular signaling of Vilda was estimated by elevation of GLP-1 level and protein expressions of survival proteins; p85/p55 (pY458/199)-PI3K, pS473-Akt. Together, it boosted striatal neurotrophic factors and receptor; pS133-CREB, BDNF, pY515-TrKB, which subsequently maintained mitochondrial integrity, as indicated by enhancing both SDH and COX activities, and the redox modulators; Sirt1, Nrf2. Such neuroprotection restored imbalance of neurotransmitters through increasing GABA and suppressing glutamate as well PDE10A. These effects were reversed by WM pre-administration. In conclusion, Vilda purveyed significant anti-Huntington effect which may be mediated, at least in part, via activation of GLP-1/PI3K/Akt pathway in 3NP rat model.

Indexed as

AnimalsBehavior, AnimalBrain-Derived Neurotrophic FactorCorpus StriatumDipeptidyl-Peptidase IV InhibitorsDisease Models, AnimalGlucagon-Like Peptide-1 ReceptorHuntington DiseaseMaleMaze LearningNitro CompoundsPhosphatidylinositol 3-KinasePropionatesProto-Oncogene Proteins c-aktRats, WistarRotarod Performance Test3-nitropropionic acidBdnf protein, ratBrain-Derived Neurotrophic FactorDipeptidyl-Peptidase IV InhibitorsGlp1r protein, ratGlucagon-Like Peptide-1 ReceptorNitro CompoundsPhosphatidylinositol 3-KinasePropionatesProto-Oncogene Proteins c-aktVildagliptin3-nitropropionic acidGlucagon like peptide-1Mitochondrial dysfunctionPI3K/Akt signalingVildagliptin

Identifiers

PMID31728850
PMCPMC7007456
OpenAlexW2983216736

What Socratic holds

Textmetadata
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 Socratic graph.