Evidence map›Paper›PMID 32462551›Full record

ReviewMolecular neurobiology2020

Mitochondrial Dysfunction: a Potential Therapeutic Target to Treat Alzheimer's Disease.

Sachchida Nand Rai, Charan Singh, Arti Singh, M P Singh, Brijesh Kumar Singh

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular neurobiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 119 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
119citing papers in PubMed, 4 pooled it
7.1field-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

119 citing papers in PubMed, 4 syntheses or guidelines pooled it, 193 citations in OpenAlex.

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

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

5 authors at 3 institutions in 2 countries.

Sachchida Nand RaiCentre of Biotechnology, University of Allahabad, Prayagraj, 211002, India.
Charan SinghDepartment of Pharmaceutics ISF College of Pharmacy, Moga, Affiliated to IK Gujral Punjab Technical University, Jalandhar, Punjab, 142001, India.
Arti SinghDepartment of Pharmacology, ISF College of Pharmacy, Moga, Affiliated to IK Gujral Punjab Technical University, Jalandhar, Punjab, India.
M P SinghCentre of Biotechnology, University of Allahabad, Prayagraj, 211002, India.
Brijesh Kumar SinghDepartment of Pathology and Cell Biology, Columbia University Medical Center, New York, NY, USA. bks2139@cumc.columbia.edu.ORCID http://orcid.org/0000-0002-9689-8382
Punjab Technical University · INUniversity of Allahabad · INColumbia University Irving Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial dysfunction plays a very vital role in the pathogenesis of Alzheimer's disease (AD). Several shreds of evidence have indicated that the mitochondrial function is severely compromised under AD pathogenesis. Most of the recent therapeutic strategies have been conversed to treat AD by pinpointing the pathways involved in the pathophysiology of AD. In AD, mitochondria progressively lose their proper functions that are ultimately responsible for their accumulation and removal via the autophagic process, which is called mitophagy that further worsens the progression of this incapacitating disease. Preclinical and clinical studies have suggested that mitochondrial dysfunction along with mitophagy significantly contributes to the accumulation of amyloid-beta (Aβ) fibrils and hyperphosphorylated tau protein tangles which lead to synaptic dysfunctions and cognitive impairments such as memory loss through reactive oxygen species (ROS)-mediated pathway. The present review is intended to discuss the recent advancements in the frontiers of mitochondrial dysfunction and consequent therapeutic strategies that have been employed to treat AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsBrainHumansMitochondriaOxidative StressPhosphorylationReactive Oxygen Speciestau ProteinsAmyloid beta-PeptidesReactive Oxygen Speciestau ProteinsAlzheimer’s diseaseAutophagyMitochondrial dysfunctionMitophagy

Identifiers

PMID32462551
OpenAlexW3029009649

What OpenQuestion 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 OpenQuestion graph.