Evidence map›Paper›PMID 32392471›Full record

ArticleNeuron2020

SEQUIN Multiscale Imaging of Mammalian Central Synapses Reveals Loss of Synaptic Connectivity Resulting from Diffuse Traumatic Brain Injury.

Andrew D Sauerbeck, Mihika Gangolli, Sydney J Reitz, Maverick H Salyards, Samuel H Kim, Christopher Hemingway, Maud Gratuze, Tejaswi Makkapati, Martin Kerschensteiner, David M Holtzman and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Neuron, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

34 citing papers in PubMed, 47 citations in OpenAlex.

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  17. Super-Resolution Vibrational Imaging Using Expansion Stimulated Raman Scattering Microscopy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022
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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

12 authors at 4 institutions in 2 countries.

Andrew D SauerbeckDepartment of Neurology, Hope Center for Neurological Disorders, Knight Alzheimer's Disease Research Center, Washington University School of Medicine, St. Louis, MO 63110, USA.
Mihika GangolliMcKelvey School of Engineering, Washington University, St. Louis, MO 63130, USA; Currently, Center for Neuroscience and Regenerative Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA.
Sydney J ReitzDepartment of Neurology, Hope Center for Neurological Disorders, Knight Alzheimer's Disease Research Center, Washington University School of Medicine, St. Louis, MO 63110, USA.
Maverick H SalyardsDepartment of Neurology, Hope Center for Neurological Disorders, Knight Alzheimer's Disease Research Center, Washington University School of Medicine, St. Louis, MO 63110, USA.
Samuel H KimDepartment of Neurology, Hope Center for Neurological Disorders, Knight Alzheimer's Disease Research Center, Washington University School of Medicine, St. Louis, MO 63110, USA.
Christopher HemingwayInstitute of Clinical Neuroimmunology, Ludwig-Maximilians Universität München, Munich 82152, Germany.
Maud GratuzeDepartment of Neurology, Hope Center for Neurological Disorders, Knight Alzheimer's Disease Research Center, Washington University School of Medicine, St. Louis, MO 63110, USA.
Tejaswi MakkapatiDepartment of Neurology, Hope Center for Neurological Disorders, Knight Alzheimer's Disease Research Center, Washington University School of Medicine, St. Louis, MO 63110, USA.
Martin KerschensteinerInstitute of Clinical Neuroimmunology, Ludwig-Maximilians Universität München, Munich 82152, Germany; Munich Cluster of Systems Neurology (SyNergy), Munich 81377, Germany.
David M HoltzmanDepartment of Neurology, Hope Center for Neurological Disorders, Knight Alzheimer's Disease Research Center, Washington University School of Medicine, St. Louis, MO 63110, USA.
David L BrodyDepartment of Neurology, Hope Center for Neurological Disorders, Knight Alzheimer's Disease Research Center, Washington University School of Medicine, St. Louis, MO 63110, USA; Currently, Center for Neuroscience and Regenerative Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA.
Terrance T KummerDepartment of Neurology, Hope Center for Neurological Disorders, Knight Alzheimer's Disease Research Center, Washington University School of Medicine, St. Louis, MO 63110, USA. Electronic address: kummert@wustl.edu.
Hope Center for Neurological Disorders · USUniformed Services University of the Health Sciences · USLudwig-Maximilians-Universität München · DEMunich Cluster for Systems Neurology · DE

Funding

ADVANCED DIFFUSION BIOMARKERS OF BRAIN INJURY IN SUBARACHNOID HEMORRHAGEK08NS094760 · NINDS · WASHINGTON UNIVERSITY · PI KUMMER, TERRANCE T · 2015 to 2018
$680k
ZEISS LSM880 AIRYSCAN MICROSCOPE FOR SHARED BIOMEDICAL RESEARCHS10OD021629 · OD · WASHINGTON UNIVERSITY · PI FITZPATRICK, JAMES ALEXANDER · 2017 to 2017
$596k
Unbiased High Content Screening for Novel Synaptotoxic Substances in Human Alzheimer's Disease Brain LysatesR21NS102983 · NINDS · WASHINGTON UNIVERSITY · PI KUMMER, TERRANCE T · 2017 to 2018
$419k
NIH HHS S10 OD021629NINDS NIH HHS K08 NS094760NINDS NIH HHS R21 NS102983
6 · The paper itself

Abstract

The brain's complex microconnectivity underlies its computational abilities and vulnerability to injury and disease. It has been challenging to illuminate the features of this synaptic network due to the small size and dense packing of its elements. Here, we describe a rapid, accessible super-resolution imaging and analysis workflow-SEQUIN-that quantifies central synapses in human tissue and animal models, characterizes their nanostructural and molecular features, and enables volumetric imaging of mesoscale synaptic networks without the production of large histological arrays. Using SEQUIN, we identify cortical synapse loss resulting from diffuse traumatic brain injury, a highly prevalent connectional disorder. Similar synapse loss is observed in three murine models of Alzheimer-related neurodegeneration, where SEQUIN mesoscale mapping identifies regional synaptic vulnerability. These results establish an easily implemented and robust nano-to-mesoscale synapse quantification and characterization method. They furthermore identify a shared mechanism-synaptopathy-between Alzheimer neurodegeneration and its best-established epigenetic risk factor, brain trauma.

Indexed as

AnimalsBrain Injuries, TraumaticBrain MappingCentral Nervous SystemCerebral CortexHumansMammalsMiceNanostructuresNeural PathwaysNeuroimagingSynapsesAlzheimer’s diseaseimagingmicroconnectivityneurodegenerationSEQUINsuper-resolution microscopysynapsesynaptomeTBItraumatic brain injury

Identifiers

PMID32392471
PMCPMC7381374
OpenAlexW3022125061

What OpenQuestion holds

Textmetadata
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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.