Evidence map›Paper›PMID 36043795›Full record

ReviewCurrent neuropharmacology2023

Mitochondrial Medicine: A Promising Therapeutic Option Against Various Neurodegenerative Disorders.

Mohannad A Almikhlafi, Mohammed M Karami, Ankit Jana, Thamer M Alqurashi, Mohammed Majrashi, Badrah S Alghamdi, Ghulam Md Ashraf

Open access · greenAbstract readReview
In one paragraph

Review in Current neuropharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

15 citing papers in PubMed, 22 citations in OpenAlex.

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  14. The role of exercise in Parkinson's Disease.Neurosciences (Riyadh, Saudi Arabia) · 2023
    Review
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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

7 authors at 5 institutions in 3 countries.

Mohannad A AlmikhlafiDepartment of Pharmacology and Toxicology, College of Pharmacy, Taibah University, Madinah, Saudi Arabia.
Mohammed M KaramiDepartment of Physiology, Neuroscience Unit, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia.
Ankit JanaSchool of Biotechnology, Kalinga Institute of Industrial Technology (KIIT) Deemed to be University, Campus-11, Patia, Bhubaneswar, Odisha, 751024, India.
Thamer M AlqurashiDepartment of Pharmacology, Faculty of Medicine, Rabigh, King Abdulaziz University, Jeddah, Saudi Arabia.
Mohammed MajrashiDepartment of Pharmacology, Faculty of Medicine, University of Jeddah, Jeddah, Saudi Arabia.
Badrah S AlghamdiDepartment of Physiology, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia.
Ghulam Md AshrafDepartment of Medical Laboratory Sciences, College of Health Sciences, University of Sharjah, University City, Sharjah 27272, United Arab Emirates.
King Abdulaziz University · SAJeddah University · SAKIIT University · INTaibah University · SAUniversity of Sharjah · AE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Abnormal mitochondrial morphology and metabolic dysfunction have been observed in many neurodegenerative disorders (NDDs). Mitochondrial dysfunction can be caused by aberrant mitochondrial DNA, mutant nuclear proteins that interact with mitochondria directly or indirectly, or for unknown reasons. Since mitochondria play a significant role in neurodegeneration, mitochondriatargeted therapies represent a prosperous direction for the development of novel drug compounds that can be used to treat NDDs. This review gives a brief description of how mitochondrial abnormalities lead to various NDDs such as Alzheimer's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis. We further explore the promising therapeutic effectiveness of mitochondria- directed antioxidants, MitoQ, MitoVitE, MitoPBN, and dimebon. We have also discussed the possibility of mitochondrial gene therapy as a therapeutic option for these NDDs.

Indexed as

Alzheimer DiseaseNeurodegenerative DiseasesParkinson DiseaseDNA, MitochondrialHumansMitochondriaDNA, MitochondrialAlzheimer’s diseaseamyotrophic lateral sclerosisgene therapyHuntington’s diseasemitochondrial dysfunctionParkinson’s disease

Identifiers

PMID36043795
PMCPMC10286591
OpenAlexW4293560934

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.