Evidence map›Paper›PMID 25511986›Full record

ArticleScientific reports2014

Levodopa/benserazide microsphere (LBM) prevents L-dopa induced dyskinesia by inactivation of the DR1/PKA/P-tau pathway in 6-OHDA-lesioned Parkinson's rats.

Cheng-long Xie, Wen-Wen Wang, Su-fang Zhang, Ming-Lu Yuan, Jun-Yi Che, Jing Gan, Lu Song, Wei-En Yuan, Zhen-Guo Liu

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.6field-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

21 citing papers in PubMed, 30 citations in OpenAlex.

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  11. DOPA Decarboxylase Modulates Tau Toxicity.Biological psychiatry · 2018
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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

9 authors at 2 institutions in 1 country.

Cheng-long XieDepartment of Neurology, Xinhua Hospital affiliated to the Medical School of Shanghai Jiaotong University, 200092, 1665 Kongjiang Road, Shanghai, China.
Wen-Wen WangThe center of Traditional Chinese Medicine, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou 325027, China.
Su-fang ZhangDepartment of Neurology, Xinhua Hospital affiliated to the Medical School of Shanghai Jiaotong University, 200092, 1665 Kongjiang Road, Shanghai, China.
Ming-Lu YuanSchool of Pharmacy, Shanghai Jiaotong University, Shanghai 200240, China.
Jun-Yi CheSchool of Pharmacy, Shanghai Jiaotong University, Shanghai 200240, China.
Jing GanDepartment of Neurology, Xinhua Hospital affiliated to the Medical School of Shanghai Jiaotong University, 200092, 1665 Kongjiang Road, Shanghai, China.
Lu SongDepartment of Neurology, Xinhua Hospital affiliated to the Medical School of Shanghai Jiaotong University, 200092, 1665 Kongjiang Road, Shanghai, China.
Wei-En YuanSchool of Pharmacy, Shanghai Jiaotong University, Shanghai 200240, China.
Zhen-Guo LiuDepartment of Neurology, Xinhua Hospital affiliated to the Medical School of Shanghai Jiaotong University, 200092, 1665 Kongjiang Road, Shanghai, China.
XinHua Hospital · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

L-3, 4-dihydroxyphenylalanine (L-dopa) is the gold standard for symptomatic treatment of Parkinson's disease (PD), but long-term therapy is associated with the emergence of L-dopa-induced dyskinesia (LID). In the present study, L-dopa and benserazide were loaded by poly (lactic-co-glycolic acid) microspheres (LBM), which can release levodopa and benserazide in a sustained manner in order to continuous stimulate dopaminergic receptors. We investigated the role of striatal DR1/PKA/P-tau signal transduction in the molecular event underlying LID in the 6-OHDA-lesioned rat model of PD. We found that animals rendered dyskinetic by L-dopa treatment, administration of LBM prevented the severity of AIM score, as well as improvement in motor function. Moreover, we also showed L-dopa elicits profound alterations in the activity of three LID molecular markers, namely DR1/PKA/P-tau (ser396). These modifications are totally prevented by LBM treatment, a similar way to achieve continuous dopaminergic delivery (CDD). In conclusion, our experiments provided evidence that intermittent administration of L-dopa, but not continuous delivery, and DR1/PKA/p-tau (ser396) activation played a critical role in the molecular and behavioural induction of LID in 6-OHDA-lesioned rats. In addition, LBM treatment prevented the development of LID by inhibiting the expression of DR1/PKA/p-tau, as well as PPEB mRNA in dyskintic rats.

Indexed as

Adrenergic AgentsAnimalsBenserazideBlotting, WesternCorpus StriatumCyclic AMP-Dependent Protein KinasesDopamine AgentsDrug CombinationsDyskinesiasFemaleFluorescent Antibody TechniqueLactic AcidLevodopaMicrospheresNeuronsOxidopamineAdrenergic AgentsBenserazidebenserazide, levodopa drug combinationCyclic AMP-Dependent Protein KinasesDopamine Agentsdown-regulator of transcription 1Drug CombinationsLactic AcidLevodopaMapt protein, ratOxidopaminePhosphoproteinsPolyglycolic AcidPolylactic Acid-Polyglycolic Acid CopolymerRNA, Messengertau ProteinsTranscription Factors

Identifiers

PMID25511986
PMCPMC4267205
OpenAlexW2073681259

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.