Evidence map›Paper›PMID 23225012›Full record

ReviewSub-cellular biochemistry2012

Parkinson's disease.

Timothy R Mhyre, James T Boyd, Robert W Hamill, Kathleen A Maguire-Zeiss

2 registry-linked trialsAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Sub-cellular biochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 178 papers, 9 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
178citing papers in PubMed, 9 pooled it
5.8field-weighted citation impact, top 3% 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.

NCT04837313 naunknown statusnot on this mapstarted 2021, after this paper: background citation

Efficacy and Safety of Fecal Microbiota Transplantation in the Treatment of Parkinson's Disease With Constipation

TypeinterventionalSponsorGuangzhou First People's HospitalRan2021 to 2025Enrolled30ConditionsParkinson's Disease, Fecal Microbiota TransplantationArmsFecal Microbiota Transplantation
NCT05444907 recruitingnot on this mapstarted 2021, after this paper: background citation

Understanding Deep Brain Stimulation-induced Mania: Finding Potential Predictors to Optimize Treatment

TypeobservationalSponsorAlbino MaiaRan2021 to 2025Enrolled100ConditionsMania, Parkinson DiseaseArmsNo Intervention / Exposure
3 · Its place in the literature

Who cites it

178 citing papers in PubMed, 9 syntheses or guidelines pooled it, 424 citations in OpenAlex.

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  4. Impulse control disorders in Parkinson's disease patients treated with pramipexole and ropinirole: a systematic review and meta-analysis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2024
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118 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

4 authors at 3 institutions in 1 country.

Timothy R MhyreDepartment of Neuroscience, Georgetown University Medical Center, 3970 Reservoir Road, NW NRB WP-24A, 20057, Washington, DC, USA, trm36@georgetown.edu.
James T Boyd
Robert W Hamill
Kathleen A Maguire-Zeiss
University of Vermont · USGeorgetown University · USGeorgetown University Medical Center · US

Funding

Toxicant, oxidative injury, dopamine & synuclein in PDR01ES014470 · NIEHS · UNIVERSITY OF ROCHESTER · PI MAGUIRE-ZEISS, KATHLEEN ANNE · 2007 to 2011
$1.7M
NIEHS NIH HHS R01 ES014470NIEHS NIH HHS R01ES014470
6 · The paper itself

Abstract

Parkinson's disease (PD) is the most common age-related motoric neurodegenerative disease initially described in the 1800's by James Parkinson as the 'Shaking Palsy'. Loss of the neurotransmitter dopamine was recognized as underlying the pathophysiology of the motor dysfunction; subsequently discovery of dopamine replacement therapies brought substantial symptomatic benefit to PD patients. However, these therapies do not fully treat the clinical syndrome nor do they alter the natural history of this disorder motivating clinicians and researchers to further investigate the clinical phenotype, pathophysiology/pathobiology and etiology of this devastating disease. Although the exact cause of sporadic PD remains enigmatic studies of familial and rare toxicant forms of this disorder have laid the foundation for genome wide explorations and environmental studies. The combination of methodical clinical evaluation, systematic pathological studies and detailed genetic analyses have revealed that PD is a multifaceted disorder with a wide-range of clinical symptoms and pathology that include regions outside the dopamine system. One common thread in PD is the presence of intracytoplasmic inclusions that contain the protein, α-synuclein. The presence of toxic aggregated forms of α-synuclein (e.g., amyloid structures) are purported to be a harbinger of subsequent pathology. In fact, PD is both a cerebral amyloid disease and the most common synucleinopathy, that is, diseases that display accumulations of α-synuclein. Here we present our current understanding of PD etiology, pathology, clinical symptoms and therapeutic approaches with an emphasis on misfolded α-synuclein.

Indexed as

alpha-SynucleinAmyloidLewy BodiesParkinson DiseaseProteostasis DeficienciesAnimalsDopamineHumansalpha-SynucleinAmyloidDopamine

Identifiers

PMID23225012
PMCPMC4372387
OpenAlexW4205416135

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.