Evidence map›Paper›PMID 27599210›Full record

ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2017

DNP, mitochondrial uncoupling, and neuroprotection: A little dab'll do ya.

John G Geisler, Krisztina Marosi, Joshua Halpern, Mark P Mattson

Abstract read
In one paragraph

Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

63 citing papers in PubMed, 100 citations in OpenAlex.

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3 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

4 authors at 3 institutions in 1 country.

John G GeislerMitochon Pharmaceuticals, Inc., Radnor, PA, USA.
Krisztina MarosiLaboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD, USA.
Joshua HalpernLaboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD, USA.
Mark P MattsonLaboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD, USA; Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Electronic address: mark.mattson@nih.gov.
National Institute on Aging · USInstitute on Aging · USMarinus Pharmaceuticals (United States) · US

Funding

Neuroprotective And Neurorestorative Signaling Mechanisms in Alzheimer's DiseaseZIAAG000314 · NIA · NATIONAL INSTITUTE ON AGING · PI MATTSON, MARK · 2009 to 2018
$6.7M
Cellular And Molecular Pathogenesis Of Alzheimer's DiseaseZIAAG000312 · NIA · NATIONAL INSTITUTE ON AGING · PI MATTSON, MARK · 2009 to 2018
$6.4M
Apoptosis In Neurodegenerative DisordersZIAAG000313 · NIA · NATIONAL INSTITUTE ON AGING · PI MATTSON, MARK · 2009 to 2018
$6.4M
Hormesis/Adaptive Stress Responses and AgingZIAAG000331 · NIA · NATIONAL INSTITUTE ON AGING · PI MATTSON, MARK · 2009 to 2018
$5.0M
Intramural NIH HHS ZIA AG000312Intramural NIH HHS ZIA AG000314
6 · The paper itself

Abstract

Recent findings have elucidated roles for mitochondrial uncoupling proteins (UCPs) in neuronal plasticity and resistance to metabolic and oxidative stress. UCPs are induced by bioenergetic challenges such as caloric restriction and exercise and may protect neurons against dysfunction and degeneration. The pharmacological uncoupler 2,4-dinitrophenol (DNP), which was once prescribed to >100,000 people as a treatment for obesity, stimulates several adaptive cellular stress-response signaling pathways in neurons including those involving the brain-derived neurotrophic factor (BDNF), the transcription factor cyclic AMP response element-binding protein (CREB), and autophagy. Preclinical data show that low doses of DNP can protect neurons and improve functional outcome in animal models of Alzheimer's and Parkinson's diseases, epilepsy, and cerebral ischemic stroke. Repurposing of DNP and the development of novel uncoupling agents with hormetic mechanisms of action provide opportunities for new breakthrough therapeutic interventions in a range of acute and chronic insidious neurodegenerative/neuromuscular conditions, all paradoxically at body weight-preserving doses.

Indexed as

2,4-DinitrophenolAnimalsBrain-Derived Neurotrophic FactorDisease Models, AnimalHumansNeurodegenerative DiseasesNeuronal PlasticityNeuroprotectionUncoupling Protein 12,4-DinitrophenolBrain-Derived Neurotrophic FactorUncoupling Protein 1BDNFCREBDNPHormesisMitochondrial uncouplingParkinson's diseaseSynaptic plasticity

Identifiers

PMID27599210
PMCPMC5337177
OpenAlexW2515018235

What OpenQuestion holds

Textmetadata
LicenceTDM
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.