Evidence map›Paper›PMID 31222062›Full record

ReviewNature reviews. Neurology2019

SILK studies - capturing the turnover of proteins linked to neurodegenerative diseases.

Ross W Paterson, Audrey Gabelle, Brendan P Lucey, Nicolas R Barthélemy, Claire A Leckey, Christophe Hirtz, Sylvain Lehmann, Chihiro Sato, Bruce W Patterson, Tim West and 11 more

Open access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Neurology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

44 citing papers in PubMed, 67 citations in OpenAlex.

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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

21 authors at 7 institutions in 4 countries.

Ross W PatersonDementia Research Centre, Department of Neurodegeneration, University College London (UCL) Institute of Neurology, London, UK. r.paterson@ucl.ac.uk.ORCID http://orcid.org/0000-0001-9372-3635
Audrey GabelleDepartment of Neurology, Memory Research and Resources Centre, Centre Hospitalier Universitaire (CHU), Montpellier, France.
Brendan P LuceyDepartment of Neurology, Washington University School of Medicine, St Louis, MO, USA.
Nicolas R BarthélemyDepartment of Neurology, Washington University School of Medicine, St Louis, MO, USA.
Claire A LeckeyDepartment of Neurodegenerative Disease, University College London (UCL) Institute of Neurology, London, UK.
Christophe HirtzDepartment of Neurology, Memory Research and Resources Centre, Centre Hospitalier Universitaire (CHU), Montpellier, France.
Sylvain LehmannDepartment of Neurology, Memory Research and Resources Centre, Centre Hospitalier Universitaire (CHU), Montpellier, France.
Chihiro SatoDepartment of Neurology, Washington University School of Medicine, St Louis, MO, USA.ORCID http://orcid.org/0000-0002-7639-8727
Bruce W PattersonDepartment of Medicine, Washington University School of Medicine, St Louis, MO, USA.
Tim WestC2N Diagnostics, Center for Emerging Technologies, St Louis, MO, USA.ORCID http://orcid.org/0000-0003-3267-8249
Kevin YarasheskiC2N Diagnostics, Center for Emerging Technologies, St Louis, MO, USA.
Jonathan D RohrerDementia Research Centre, Department of Neurodegeneration, University College London (UCL) Institute of Neurology, London, UK.
Norelle C WildburgerDepartment of Neurology, Washington University School of Medicine, St Louis, MO, USA.ORCID http://orcid.org/0000-0002-0036-8927
Jonathan M SchottDementia Research Centre, Department of Neurodegeneration, University College London (UCL) Institute of Neurology, London, UK.ORCID http://orcid.org/0000-0003-2059-024X
Celeste M KarchDepartment of Psychiatry, Washington University, St Louis, MO, USA.ORCID http://orcid.org/0000-0002-6854-5547
Selina WrayDepartment of Neurodegenerative Disease, University College London (UCL) Institute of Neurology, London, UK.
Timothy M MillerDepartment of Neurology, Washington University School of Medicine, St Louis, MO, USA.
Donald L ElbertDepartment of Neurology, Dell Medical School, University of Texas at Austin, Austin, TX, USA.
Henrik ZetterbergDementia Research Centre, Department of Neurodegeneration, University College London (UCL) Institute of Neurology, London, UK.
Nick C FoxDementia Research Centre, Department of Neurodegeneration, University College London (UCL) Institute of Neurology, London, UK.
Randall J BatemanDepartment of Neurology, Washington University School of Medicine, St Louis, MO, USA.
Washington University in St. Louis · USUK Dementia Research Institute · GBInserm · FRC2N Diagnostics (United States) · USUniversity College London · GBSahlgrenska University Hospital · SEThe University of Texas at Austin · US

Funding

CNS and Plasma Amyloid--Beta Kinetics in Alzheimer's DiseaseR01NS065667 · NINDS · WASHINGTON UNIVERSITY · PI BATEMAN, RANDALL J · 2008 to 2016
$4.6M
CNS TAU KINETICS IN ALZHEIMER'S DISEASER01NS095773 · NINDS · WASHINGTON UNIVERSITY · PI BATEMAN, RANDALL J · 2016 to 2020
$3.6M
Understanding SOD1 Kinetics in Amyotrophic Lateral SclerosisR01NS097816 · NINDS · WASHINGTON UNIVERSITY · PI MILLER, TIMOTHY M. · 2016 to 2018
$1.7M
SLEEP QUALITY AND HUMAN AMLYOID-BETA KINETICSK76AG054863 · NIA · WASHINGTON UNIVERSITY · PI LUCEY, BRENDAN PATRICK · 2016 to 2020
$982k
GENETIC DISRUPTION OF TAU METABOLISM IN TAUOPATHIESK01AG046374 · NIA · WASHINGTON UNIVERSITY · PI KARCH, CELESTE MARIE · 2014 to 2018
$568k
Spleen glia in autonomic regulation of immunityR21NS098716 · NINDS · STANFORD UNIVERSITY · PI BUCKWALTER, MARION S · 2016 to 2017
$454k
NIA NIH HHS K01 AG046374NIA NIH HHS K76 AG054863NINDS NIH HHS R01 NS065667NINDS NIH HHS R01 NS095773NINDS NIH HHS R01 NS097816NINDS NIH HHS R21 NS098716
6 · The paper itself

Abstract

Alzheimer disease (AD) is one of several neurodegenerative diseases characterized by dysregulation, misfolding and accumulation of specific proteins in the CNS. The stable isotope labelling kinetics (SILK) technique is based on generating amino acids labelled with naturally occurring stable (that is, nonradioactive) isotopes of carbon and/or nitrogen. These labelled amino acids can then be incorporated into proteins, enabling rates of protein production and clearance to be determined in vivo and in vitro without the use of radioactive or chemical labels. Over the past decade, SILK studies have been used to determine the turnover of key pathogenic proteins amyloid-β (Aβ), tau and superoxide dismutase 1 (SOD1) in the cerebrospinal fluid of healthy individuals, patients with AD and those with other neurodegenerative diseases. These studies led to the identification of several factors that alter the production and/or clearance of these proteins, including age, sleep and disease-causing genetic mutations. SILK studies have also been used to measure Aβ turnover in blood and within brain tissue. SILK studies offer the potential to elucidate the mechanisms underlying various neurodegenerative disease mechanisms, including neuroinflammation and synaptic dysfunction, and to demonstrate target engagement of novel disease-modifying therapies.

Indexed as

Isotope LabelingAmyloid beta-PeptidesBrainHumansNeurodegenerative Diseasestau ProteinsAmyloid beta-Peptidestau Proteins

Identifiers

PMID31222062
PMCPMC6876864
OpenAlexW2949287877

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.