Evidence map›Paper›PMID 31818365›Full record

ReviewBMB reports2020

Mitochondrial dysfunction and Alzheimer's disease: prospects for therapeutic intervention.

Ji Woong Lim, Jiyoun Lee, Ae Nim Pae

Abstract readReview
In one paragraph

Review in BMB reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

22 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  5. Trilostane: Beyond Cushing's Syndrome.Animals : an open access journal from MDPI · 2025
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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

3 authors.

Ji Woong LimConvergence Research Center for Diagnosis, Treatment and Care System of Dementia, Korea Institute of Science and Technology, Seoul 02792, Korea.
Jiyoun LeeDepartment of Global Medical Science, Sungshin University, Seoul 01133, Korea.
Ae Nim PaeConvergence Research Center for Diagnosis, Treatment and Care System of Dementia, Korea Institute of Science and Technology, Seoul 02792; Division of Bio-Medical Science & Technology, KIST School, Korea University of Science and Technology, Seoul 02792, Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a multifactorial neurodegenerative disease and has become a major socioeconomic issue in many developed countries. Currently available therapeutic agents for AD provide only symptomatic treatments, mainly because the complete mechanism of the AD pathogenesis is still unclear. Although several different hypotheses have been proposed, mitochondrial dysfunction has gathered interest because of its profound effect on brain bioenergetics and neuronal survival in the pathophysiology of AD. Various therapeutic agents targeting the mitochondrial pathways associated with AD have been developed over the past decade. Although most of these agents are still early in the clinical development process, they are used to restore mitochondrial function, which provides an alternative therapeutic strategy that is likely to slow the progression of the disease. In this mini review, we will survey the AD-related mitochondrial pathways and their small-molecule modulators that have therapeutic potential. We will focus on recently reported examples, and also overview the current challenges and future perspectives of ongoing research. [BMB Reports 2020; 53(1): 47-55].

Indexed as

17-Hydroxysteroid Dehydrogenases3-Hydroxyacyl CoA DehydrogenasesAlzheimer DiseaseAnimalsBrainDisease ProgressionDynaminsHumansMitochondriaMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreMitochondrial ProteinsNeurosteroidsOxidative StressProtein KinasesPTEN-Induced Putative Kinase17-Hydroxysteroid Dehydrogenases3-Hydroxyacyl CoA DehydrogenasesDNM1L protein, humanDynaminsHSD17B10 protein, humanMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreMitochondrial ProteinsNeurosteroidsProtein KinasesPTEN-Induced Putative KinaseReceptors, GABATSPO protein, human

Identifiers

PMID31818365
PMCPMC6999825

What OpenQuestion holds

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LicenceCC BY-NC
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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.