Evidence map›Paper›PMID 24594681›Full record

ArticlePloS one2014

Increased precursor cell proliferation after deep brain stimulation for Parkinson's disease: a human study.

Vinata Vedam-Mai, Bronwen Gardner, Michael S Okun, Florian A Siebzehnrubl, Monica Kam, Palingu Aponso, Dennis A Steindler, Anthony T Yachnis, Dan Neal, Brittany U Oliver and 4 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 6% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.

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  17. Glial responses to implanted electrodes in the brain.Nature biomedical engineering · 2017
    Article
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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

14 authors at 2 institutions in 2 countries.

Vinata Vedam-MaiDepartment of Neurosurgery, McKnight Brain Institute, University of Florida, Gainesville, Florida, United States of America; Department of Neurology, UF Center for Movement Disorders and Restoration, University of Florida, Gainesville, Florida, United States of America.
Bronwen GardnerDepartment of Anatomy with Radiology and Centre for Brain Research, School of Medical and Health Sciences, The University of Auckland, Auckland, New Zealand.
Michael S OkunDepartment of Neurosurgery, McKnight Brain Institute, University of Florida, Gainesville, Florida, United States of America; Department of Neurology, UF Center for Movement Disorders and Restoration, University of Florida, Gainesville, Florida, United States of America.
Florian A SiebzehnrublDepartment of Neurosurgery, McKnight Brain Institute, University of Florida, Gainesville, Florida, United States of America.
Monica KamDepartment of Anatomy with Radiology and Centre for Brain Research, School of Medical and Health Sciences, The University of Auckland, Auckland, New Zealand.
Palingu AponsoDepartment of Anatomy with Radiology and Centre for Brain Research, School of Medical and Health Sciences, The University of Auckland, Auckland, New Zealand.
Dennis A SteindlerDepartment of Neurosurgery, McKnight Brain Institute, University of Florida, Gainesville, Florida, United States of America.
Anthony T YachnisDepartment of Pathology, University of Florida, Gainesville, Florida, United States of America.
Dan NealDepartment of Biostatistics, University of Florida, Gainesville, Florida, United States of America.
Brittany U OliverDepartment of Neurosurgery, McKnight Brain Institute, University of Florida, Gainesville, Florida, United States of America.
Sean J RathDepartment of Neurosurgery, McKnight Brain Institute, University of Florida, Gainesville, Florida, United States of America.
Richard L M FaullDepartment of Anatomy with Radiology and Centre for Brain Research, School of Medical and Health Sciences, The University of Auckland, Auckland, New Zealand.
Brent A ReynoldsDepartment of Neurosurgery, McKnight Brain Institute, University of Florida, Gainesville, Florida, United States of America.
Maurice A CurtisDepartment of Anatomy with Radiology and Centre for Brain Research, School of Medical and Health Sciences, The University of Auckland, Auckland, New Zealand.
University of Florida · USUniversity of Auckland · NZ

Funding

Research Education ComponentP30AG019610 · NIA · SUN HEALTH RESEARCH INSTITUTE · PI REIMAN, ERIC MICHAEL · 2001 to 2020
$32.5M
National Brain and Tissue Resource for Parkinson's Disease and Related DisordersU24NS072026 · NINDS · BANNER SUN HEALTH RESEARCH INSTITUTE · PI BEACH, THOMAS G · 2011 to 2015
$7.8M
NIA NIH HHS P30 AG019610NIA NIH HHS P30 AG19610NINDS NIH HHS U24 NS072026
6 · The paper itself

Abstract

objectiveDeep brain stimulation (DBS) has been used for more than a decade to treat Parkinson's disease (PD); however, its mechanism of action remains unknown. Given the close proximity of the electrode trajectory to areas of the brain known as the "germinal niches," we sought to explore the possibility that DBS influences neural stem cell proliferation locally, as well as more distantly.

methodsWe studied the brains of a total of 12 idiopathic Parkinson's disease patients that were treated with DBS (the electrode placement occurred 0.5-6 years before death), and who subsequently died of unrelated illnesses. These were compared to the brains of 10 control individuals without CNS disease, and those of 5 PD patients with no DBS.

resultsImmunohistochemical analyses of the subventricular zone (SVZ) of the lateral ventricles, the third ventricle lining, and the tissue surrounding the DBS lead revealed significantly greater numbers of proliferating cells expressing markers of the cell cycle, plasticity, and neural precursor cells in PD-DBS tissue compared with both normal brain tissue and tissue from PD patients not treated with DBS. The level of cell proliferation in the SVZ in PD-DBS brains was 2-6 fold greater than that in normal and untreated PD brains.

conclusionsOur data suggest that DBS is capable of increasing cellular plasticity in the brain, and we hypothesize that it may have more widespread effects beyond the electrode location. It is unclear whether these effects of DBS have any symptomatic or other beneficial influences on PD.

Indexed as

Cell ProliferationDeep Brain StimulationHumansImmunohistochemistryParkinson Disease

Identifiers

PMID24594681
PMCPMC3940428
OpenAlexW2009633584

What OpenQuestion holds

Textmetadata
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.