Evidence map›Paper›PMID 34751120›Full record

ReviewCurrent neuropharmacology2022

Advances in PPARs Molecular Dynamics and Glitazones as a Repurposing Therapeutic Strategy through Mitochondrial Redox Dynamics against Neurodegeneration.

Priya Durai, Narasimha M Beeraka, Hemanth Vikram Poola Ramachandrappa, Prakash Krishnan, Pranesh Gudur, Nulgumnalli Manjunathaiah Raghavendra, Prashantha Kumar Bommenahally Ravanappa

Open access · greenAbstract readReview
In one paragraph

Review in Current neuropharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 30% 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, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
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

7 authors at 3 institutions in 2 countries.

Priya DuraiDepartment of Pharmaceutical Chemistry, JSS College of Pharmacy, Mysuru 570 015, India and JSS Academy of Higher Education & Research, Mysuru, Karnataka, India.
Narasimha M BeerakaCenter of Excellence in Regenerative Medicine and Molecular Biology (CEMR), Department of Biochemistry, JSS Medical College, JSS Academy of Higher Education & Research, Mysuru 570 015, Karnataka, India.
Hemanth Vikram Poola RamachandrappaDepartment of Pharmaceutical Chemistry, JSS College of Pharmacy, Mysuru 570 015, India and JSS Academy of Higher Education & Research, Mysuru, Karnataka, India.
Prakash KrishnanIndependent Researcher, JP Nagar, Mysuru 570 015, India.
Pranesh GudurSwamy Vivekananda Yoga Anusandhana Samsthana Deemed University, Bengaluru 560 105, India.
Nulgumnalli Manjunathaiah RaghavendraDepartment of Pharmaceutical Chemistry, Acharya & BM Reddy College of Pharmacy, Bengaluru 560 107, India.
Prashantha Kumar Bommenahally RavanappaDepartment of Pharmaceutical Chemistry, JSS College of Pharmacy, Mysuru 570 015, India and JSS Academy of Higher Education & Research, Mysuru, Karnataka, India.
JSS Academy of Higher Education and Research · INSechenov University · RUSwami Vivekananda Yoga Anusandhana Samsthana · IN

Funding

Department of Science and Technology (DST), Women Scientist Scheme DST/WOS-A/CS-70/2019
6 · The paper itself

Abstract

Peroxisome proliferator-activated receptors (PPARs) activity has significant implications for the development of novel therapeutic modalities against neurodegenerative diseases. Although PPAR-α, PPAR-β/δ, and PPAR-γ nuclear receptor expressions are significantly reported in the brain, their implications in brain physiology and other neurodegenerative diseases still require extensive studies. PPAR signaling can modulate various cell signaling mechanisms involved in the cells contributing to on- and off-target actions selectively to promote therapeutic effects as well as the adverse effects of PPAR ligands. Both natural and synthetic ligands for the PPARα, PPARγ, and PPARβ/δ have been reported. PPARα (WY 14.643) and PPARγ agonists can confer neuroprotection by modulating mitochondrial dynamics through the redox system. The pharmacological effect of these agonists may deliver effective clinical responses by protecting vulnerable neurons from Aβ toxicity in Alzheimer's disease (AD) patients. Therefore, the current review delineated the ligands' interaction with 3D-PPARs to modulate neuroprotection, and also deciphered the efficacy of numerous drugs, viz. Aβ aggregation inhibitors, vaccines, and γ-secretase inhibitors against AD; this review elucidated the role of PPAR and their receptor isoforms in neural systems, and neurodegeneration in human beings. Further, we have substantially discussed the efficacy of PPREs as potent transcription factors in the brain, and the role of PPAR agonists in neurotransmission, PPAR gamma coactivator-1α (PGC-1α) and mitochondrial dynamics in neuroprotection during AD conditions. This review concludes with the statement that the development of novel PPARs agonists may benefit patients with neurodegeneration, mainly AD patients, which may help mitigate the pathophysiology of dementia, subsequently improving overall the patient's quality of life.

Indexed as

Alzheimer DiseaseNeurodegenerative DiseasesThiazolidinedionesDrug RepositioningHumansLigandsMitochondrial DynamicsMolecular Dynamics SimulationOxidation-ReductionPPAR alphaPPAR gammaQuality of LifeLigandsPPAR alphaPPAR gammaThiazolidinedionesAlzheimer’s diseaseglitazonesmitochondrial dynamicsneurodegenerationneuroinflammationPPARs

Identifiers

PMID34751120
PMCPMC9881103
OpenAlexW3211688988

What OpenQuestion holds

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LicenceCC BY-NC
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.