Evidence map›Paper›PMID 37904733›Full record

ArticleFrontiers in cellular neuroscience2023

The AMPK activator metformin improves recovery from demyelination by shifting oligodendrocyte bioenergetics and accelerating OPC differentiation.

Mohanlall Narine, Maryam A Azmi, Martin Umali, Ashley Volz, Holly Colognato

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

14 citing papers in PubMed, 16 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

5 authors at 1 institution in 1 country.

Mohanlall NarineDepartment of Pharmacological Sciences, Stony Brook University, Stony Brook, NY, United States.
Maryam A AzmiDepartment of Pharmacological Sciences, Stony Brook University, Stony Brook, NY, United States.
Martin UmaliDepartment of Pharmacological Sciences, Stony Brook University, Stony Brook, NY, United States.
Ashley VolzDepartment of Pharmacological Sciences, Stony Brook University, Stony Brook, NY, United States.
Holly ColognatoDepartment of Pharmacological Sciences, Stony Brook University, Stony Brook, NY, United States.
Stony Brook University · US

Funding

Abnormalities in postnatal brain development as a feature of congenital muscular dystrophiesR21NS114769 · NINDS · STATE UNIVERSITY NEW YORK STONY BROOK · PI COLOGNATO, HOLLY A · 2020 to 2021
$510k
NINDS NIH HHS R21 NS114769
6 · The paper itself

Abstract

Multiple Sclerosis (MS) is a chronic disease characterized by immune-mediated destruction of myelinating oligodendroglia in the central nervous system. Loss of myelin leads to neurological dysfunction and, if myelin repair fails, neurodegeneration of the denuded axons. Virtually all treatments for MS act by suppressing immune function, but do not alter myelin repair outcomes or long-term disability. Excitingly, the diabetes drug metformin, a potent activator of the cellular "energy sensor" AMPK complex, has recently been reported to enhance recovery from demyelination. In aged mice, metformin can restore responsiveness of oligodendrocyte progenitor cells (OPCs) to pro-differentiation cues, enhancing their ability to differentiate and thus repair myelin. However, metformin's influence on young oligodendroglia remains poorly understood. Here we investigated metformin's effect on the temporal dynamics of differentiation and metabolism in young, healthy oligodendroglia and in oligodendroglia following myelin damage in young adult mice. Our findings reveal that metformin accelerates early stages of myelin repair following cuprizone-induced myelin damage. Metformin treatment of both isolated OPCs and oligodendrocytes altered cellular bioenergetics, but in distinct ways,

Indexed as

cuprizonemetabolismmetforminmultiple sclerosismyelin repairoligodendrocyte

Identifiers

PMID37904733
PMCPMC10613472
OpenAlexW4387572874

What OpenQuestion holds

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LicenceCC BY
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.