Evidence map›Paper›PMID 20671245›Full record

ArticleStroke2010

Niacin treatment of stroke increases synaptic plasticity and axon growth in rats.

Xu Cui, Michael Chopp, Alex Zacharek, Cynthia Roberts, Benjamin Buller, Madalina Ion, Jieli Chen

Open access · bronzeAbstract read
In one paragraph

Article in Stroke, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

40 citing papers in PubMed, 74 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

7 authors at 1 institution in 1 country.

Xu CuiDepartment of Neurology, Henry Ford Hospital, Detroit, Mich 48202, USA.
Michael Chopp
Alex Zacharek
Cynthia Roberts
Benjamin Buller
Madalina Ion
Jieli Chen
Oakland University · US

Funding

PREDICTION OF HUMAN BRAIN INFARCTION BY MRIP01NS023393 · NINDS · HENRY FORD HOSPITAL · PI ZHANG, ZHENG GANG · 1986 to 2011
$11.0M
Neurorestorative therapy of stroke with agents that increase HDLR01AG031811 · NIA · HENRY FORD HEALTH SYSTEM · PI CHEN, JIELI · 2009 to 2013
$1.4M
Neuroprotective therapy of stroke with HUCNC and simvastatinR41NS064708 · NINDS · SANERON CCEL THERAPEUTICS, INC. · PI CHEN, JIELI · 2010 to 2010
$177k
NIA NIH HHS R01 AG031811NIA NIH HHS R01AG031811NINDS NIH HHS 1R41NS064708NINDS NIH HHS P01 NS023393NINDS NIH HHS P01 NS23393NINDS NIH HHS R41 NS064708
6 · The paper itself

Abstract

background and purposeNiacin is the most effective medication in current clinical use for increasing high-density lipoprotein cholesterol. We tested the hypothesis that niacin treatment of stroke promotes synaptic plasticity and axon growth in the ischemic brain.

methodsMale Wistar rats were subjected to 2 hours of middle cerebral artery occlusion and treated with or without Niaspan (a prolonged-release formulation of niacin, 40 mg/kg) daily for 14 days starting 24 hours after middle cerebral artery occlusion. The expression of synaptophysin, Nogo receptor, Bielschowsky silver, brain-derived neurotrophic factor, and its receptor tropomyosin-related kinase B were measured by immunohistostaining and Western blot, respectively, in the ischemic brain. Complementing in vivo studies, primary cultured neurons were used to test the effect of niacin and high-density lipoprotein on neurite outgrowth and brain-derived neurotrophic factor/tropomyosin-related kinase B expression.

resultsNiaspan treatment of stroke significantly increased synaptophysin, Bielschowsky silver, brain-derived neurotrophic factor/tropomyosin-related kinase B expression, and decreased Nogo receptor expression in the ischemic brain compared with middle cerebral artery occlusion control animals (P<0.05, n=8/group). Niacin and high-density lipoprotein treatment significantly increased neurite outgrowth and brain-derived neurotrophic factor/tropomyosin-related kinase B expression in primary cultured neurons. Tropomyosin-related kinase B inhibitor attenuated niacin-induced neurite outgrowth (P<0.05, n=6/group).

conclusionsNiacin treatment of stroke promotes synaptic plasticity and axon growth, which is mediated, at least partially, by the brain-derived neurotrophic factor/tropomyosin-related kinase B pathways.

Indexed as

Analysis of VarianceAnimalsAxonsBlotting, WesternBrain-Derived Neurotrophic FactorCells, CulturedGPI-Linked ProteinsImmunohistochemistryMaleMyelin ProteinsNeuronal PlasticityNeuronsNiacinNogo Receptor 1RatsRats, WistarBrain-Derived Neurotrophic FactorGPI-Linked ProteinsMyelin ProteinsNiacinNogo Receptor 1Receptors, Cell SurfaceReceptors, PeptideReceptor, trkBRtn4r protein, ratSynaptophysin

Identifiers

PMID20671245
PMCPMC2932778
OpenAlexW2160479657

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Registered trials

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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.