Evidence map›Paper›PMID 33440165›Full record

ArticleCell reports2021

MCT1 Deletion in Oligodendrocyte Lineage Cells Causes Late-Onset Hypomyelination and Axonal Degeneration.

Thomas Philips, Yevgeniya A Mironova, Yan Jouroukhin, Jeannie Chew, Svetlana Vidensky, Mohamed H Farah, Mikhail V Pletnikov, Dwight E Bergles, Brett M Morrison, Jeffrey D Rothstein

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed
10.8field-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

79 citing papers in PubMed, 115 citations in OpenAlex.

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19 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

10 authors at 3 institutions in 1 country.

Thomas PhilipsDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Brain Science Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Yevgeniya A MironovaSolomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Yan JouroukhinDepartment of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Jeannie ChewDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Brain Science Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Svetlana VidenskyDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Brain Science Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Mohamed H FarahDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Mikhail V PletnikovDepartment of Physiology and Biophysics, Jacobs School of Medicine and Biomedical Sciences SUNY, University at Buffalo, Buffalo, NY 14203, USA.
Dwight E BerglesSolomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Kavli Neuroscience Discovery Institute, Johns Hopkins University, Baltimore, MD 21205, USA.
Brett M MorrisonDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Brain Science Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. Electronic address: bmorris7@jhmi.edu.
Jeffrey D RothsteinDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Brain Science Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. Electronic address: jrothstein@jhmi.edu.
Johns Hopkins Medicine · USJohns Hopkins University · USUniversity at Buffalo, State University of New York · US

Funding

Nuclear and Glial Dysfunction in NeurodegenerationR35NS132179 · NINDS · JOHNS HOPKINS UNIVERSITY · PI Jeffrey D Rothstein · 2023 to 2026
$4.9M
Oligodendroglial Dysfunction in C9orf72 ALS and FTDR01NS099320 · NINDS · JOHNS HOPKINS UNIVERSITY · PI MORRISON, BRETT M., ROTHSTEIN, JEFFREY D · 2017 to 2021
$3.0M
Acquisition of a PicoQuant FLIM SystemS10OD020007 · OD · JOHNS HOPKINS UNIVERSITY · PI MCCAFFERY, J. MICHAEL · 2016 to 2016
$231k
NIH HHS S10 OD020007NINDS NIH HHS R01 NS099320NINDS NIH HHS R35 NS132179
6 · The paper itself

Abstract

Oligodendrocytes (OLs) are important for myelination and shuttling energy metabolites lactate and pyruvate toward axons through their expression of monocarboxylate transporter 1 (MCT1). Recent studies suggest that loss of OL MCT1 causes axonal degeneration. However, it is unknown how widespread and chronic loss of MCT1 in OLs specifically affects neuronal energy homeostasis with aging. To answer this, MCT1 conditional null mice were generated that allow for OL-specific MCT1 ablation. We observe that MCT1 loss from OL lineage cells is dispensable for normal myelination and axonal energy homeostasis early in life. By contrast, loss of OL lineage MCT1 expression with aging leads to significant axonal degeneration with concomitant hypomyelination. These data support the hypothesis that MCT1 is important for neuronal energy homeostasis in the aging central nervous system (CNS). The reduction in OL MCT1 that occurs with aging may enhance the risk for axonal degeneration and atrophy in neurodegenerative diseases.

Indexed as

AnimalsAxonsFemaleMaleMiceMice, TransgenicMonocarboxylate Transport Protein 1Monocarboxylic Acid TransportersMyelin SheathNerve DegenerationOligodendrogliaSymportersMonocarboxylate Transport Protein 1Monocarboxylic Acid TransportersSymportersadult onsetaxonal degenerationhypomyelinationlactatemetabolic supportmonocarboxylate transporter 1neuronoligodendrocytepyruvate

Identifiers

PMID33440165
PMCPMC8020895
OpenAlexW3119484013

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.