Evidence map›Paper›PMID 30742114›Full record

ArticleNature neuroscience2019

Mitophagy inhibits amyloid-β and tau pathology and reverses cognitive deficits in models of Alzheimer's disease.

Evandro F Fang, Yujun Hou, Konstantinos Palikaras, Bryan A Adriaanse, Jesse S Kerr, Beimeng Yang, Sofie Lautrup, Md Mahdi Hasan-Olive, Domenica Caponio, Xiuli Dan and 10 more

Open access · greenAbstract read
In one paragraph

Article in Nature neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1,021 papers.

0numbers the graph read from it
0cells of the map it votes in
1,021citing papers in PubMed
97.3field-weighted citation impact, top 1% 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

1,021 citing papers in PubMed, 1,622 citations in OpenAlex.

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

20 authors at 5 institutions in 5 countries.

Evandro F Fang *Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA. e.f.fang@medisin.uio.no.ORCID http://orcid.org/0000-0003-0355-7202
Yujun Hou *Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
Konstantinos Palikaras *Institute of Molecular Biology and Biotechnology, Foundation for Research and Technology-Hellas, Heraklion, Greece.
Bryan A AdriaanseWeatherall Institute of Molecular Medicine, University of Oxford, Oxford, UK.
Jesse S KerrLaboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
Beimeng YangLaboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
Sofie LautrupLaboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
Md Mahdi Hasan-OliveDepartment of Clinical Molecular Biology, University of Oslo and Akershus University Hospital, Lørenskog, Norway.
Domenica CaponioDepartment of Clinical Molecular Biology, University of Oslo and Akershus University Hospital, Lørenskog, Norway.ORCID http://orcid.org/0000-0002-3827-8943
Xiuli DanLaboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
Paula RocktäschelWeatherall Institute of Molecular Medicine, University of Oxford, Oxford, UK.
Deborah L CroteauLaboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
Mansour AkbariCenter for Healthy Aging, University of Copenhagen, Copenhagen, Denmark.
Nigel H GreigTranslational Gerontology Branch, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
Tormod FladbyDivision of Medicine and Laboratory Sciences, Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway.
Hilde NilsenDepartment of Clinical Molecular Biology, University of Oslo and Akershus University Hospital, Lørenskog, Norway.
M Zameel CaderWeatherall Institute of Molecular Medicine, University of Oxford, Oxford, UK.
Mark P MattsonLaboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
Nektarios TavernarakisInstitute of Molecular Biology and Biotechnology, Foundation for Research and Technology-Hellas, Heraklion, Greece.ORCID http://orcid.org/0000-0002-5253-1466
Vilhelm A BohrLaboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA. bohrv@grc.nia.nih.gov.ORCID http://orcid.org/0000-0003-4823-6429
National Institutes of Health · USUniversity of Oslo · NOUniversity of Oxford · GBUniversity of Copenhagen · DKUniversity of Crete · GR

Funding

Function of RecQ helicases in genome stabilityZ01AG000726 · NIA · NATIONAL INSTITUTE ON AGING · PI BOHR, VILHELM A · 1993 to 2008
$2.9M
Intramural NIH HHS Z01 AG000726Medical Research Council MC_PC_16034
6 · The paper itself

Abstract

Accumulation of damaged mitochondria is a hallmark of aging and age-related neurodegeneration, including Alzheimer's disease (AD). The molecular mechanisms of impaired mitochondrial homeostasis in AD are being investigated. Here we provide evidence that mitophagy is impaired in the hippocampus of AD patients, in induced pluripotent stem cell-derived human AD neurons, and in animal AD models. In both amyloid-β (Aβ) and tau Caenorhabditis elegans models of AD, mitophagy stimulation (through NAD

Indexed as

MitophagyAlzheimer DiseaseAmyloid beta-PeptidesAnimalsAnimals, Genetically ModifiedCaenorhabditis elegansDisease Models, AnimalFemaleHippocampusInduced Pluripotent Stem CellsMaleMemoryMiceNeural Stem CellsNeuronsAmyloid beta-Peptides

Identifiers

PMID30742114
PMCPMC6693625
OpenAlexW2911248861

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.