Evidence map›Paper›PMID 33486698›Full record

ArticleNeurochemical research2021

Screening of Synthetic Isoxazolone Derivative Role in Alzheimer's Disease: Computational and Pharmacological Approach.

Meissam Ali, Uzma Saleem, Fareeha Anwar, Muhammad Imran, Humaira Nadeem, Bashir Ahmad, Tahir Ali, Atta-Ur-Rehman, Tariq Ismail

Abstract read
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In one paragraph

Article in Neurochemical research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
3.9field-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

7 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Bio-Evaluation ofFrontiers in medicine · 2022
    Article
  6. Article
  7. Pharmacological Screening ofFrontiers in pharmacology · 2021
    Article
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

9 authors at 4 institutions in 1 country.

Meissam AliRiphah Institute of Pharmaceutical Sciences, Riphah International University, Lahore Campus, 54000, Pakistan.
Uzma SaleemFaculty of Pharmaceutical Sciences, Government College University, Faisalabad, 38000, Pakistan.
Fareeha AnwarRiphah Institute of Pharmaceutical Sciences, Riphah International University, Lahore Campus, 54000, Pakistan. fareeha.anwar@riphah.edu.pk.ORCID http://orcid.org/0000-0001-5097-8128
Muhammad ImranRiphah Institute of Pharmaceutical Sciences, Riphah International University, Islamabad, 44000, Pakistan.
Humaira NadeemRiphah Institute of Pharmaceutical Sciences, Riphah International University, Islamabad, 44000, Pakistan.
Bashir AhmadRiphah Institute of Pharmaceutical Sciences, Riphah International University, Lahore Campus, 54000, Pakistan.
Tahir AliRiphah Institute of Pharmaceutical Sciences, Riphah International University, Lahore Campus, 54000, Pakistan.
Atta-Ur-RehmanDepartment of Pharmacy, Faculty of Natural Sciences, Forman Chirstian College University, Ferozpur Road, Lahore, 54600, Pakistan.
Tariq IsmailDepartment of Pharmacy, COMSATS University, Abbottabad, 22060, Pakistan.
Riphah International University · PKCOMSATS University Islamabad · PKForman Christian College · PKGovernment College University, Faisalabad · PK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is age-dependent neurological disorder with progressive loss of cognition and memory. This multifactorial disease is characterized by intracellular neurofibrillary tangles, beta amyloid plaques, neuroinflammation, and increased oxidative stress. The increased cellular manifestations of these markers play a critical role in neurodegeneration and pathogenesis of AD. Therefore, reducing neurodegeneration by decreasing one or more of these markers may provide a potential therapeutic roadmap for the treatment of AD. AD causes a devastating loss of cognition with no conclusive and effective treatment. Many synthetic compound containing isoxazolone nucleus have been reported as neuroprotective agents. The aim of this study was to explore the anti-Alzheimer's potential of a newly synthesized 3,4,5-trimethoxy isoxazolone derivative (TMI) that attenuated the beta amyloid (Aβ1-42) and tau protein levels in streptozotocin (STZ) induced Alzheimer's disease mouse model. Molecular analysis revealed increased beta amyloid (Aβ1-42) protein levels, increased tau protein levels, increased cellular oxidative stress and reduced antioxidant enzymes in STZ exposed mice brains. Furthermore, ELISA and PCR were used to validate the expression of Aβ1-42. Pre-treatment with TMI significantly improved the memory and cognitive behavior along with ameliorated levels of Aβ1-42 proteins. TMI treated mice further showed marked increase in GSH, CAT, SOD levels while decreased levels of acetylcholinesterase inhibitors (AChEI's) and MDA intermediate. The multidimensional nature of isoxazolone derivatives and its versatile affinity towards various targets highpoint its multistep targeting nature. These results indicated the neuroprotective potential of TMI which may be considered for the treatment of neurodegenerative disease specifically in AD.

Indexed as

AcetylcholinesteraseAlzheimer DiseaseAmyloid beta-PeptidesAnimalsBrainDrug Evaluation, PreclinicalElevated Plus Maze TestFemaleIsoxazolesMaleMiceMolecular Docking SimulationNeuroprotective AgentsOpen Field TestPeptide FragmentsProtein BindingAcetylcholinesteraseAmyloid beta-Peptidesamyloid beta-protein (1-42)IsoxazolesNeuroprotective AgentsPeptide FragmentsStreptozocintau ProteinsAChEI’sAntioxidantBeta amyloidHippocampusIsoxazolonesOxidative stressStreptozotocin

Identifiers

PMID33486698
OpenAlexW3125008889

What OpenQuestion holds

Textmetadata
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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 OpenQuestion graph.