Evidence map›Paper›PMID 34054505›Full record

ArticleFrontiers in aging neuroscience2021

Effects of Aging on Levo-Dihydroxyphenylalanine- Induced Dyskinesia in a Rat Model of Parkinson's Disease.

Haruo Nishijima, Tamaki Kimura, Fumiaki Mori, Koichi Wakabayashi, Iku Kinoshita, Takashi Nakamura, Tomoya Kon, Chieko Suzuki, Masahiko Tomiyama

Open access · goldAbstract read
In one paragraph

Article in Frontiers in aging neuroscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.4field-weighted citation impact, top 47% 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

2 citing papers in PubMed, 7 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

9 authors at 2 institutions in 1 country.

Haruo NishijimaDepartment of Neurology, Institute of Brain Science, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Tamaki KimuraDepartment of Neurology, National Hospital Organization, Aomori Hospital, Aomori, Japan.
Fumiaki MoriDepartment of Neuropathology, Institute of Brain Science, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Koichi WakabayashiDepartment of Neuropathology, Institute of Brain Science, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Iku KinoshitaDepartment of Neurology, Institute of Brain Science, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Takashi NakamuraDepartment of Neurology, Institute of Brain Science, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Tomoya KonDepartment of Neurology, Institute of Brain Science, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Chieko SuzukiDepartment of Neurology, Institute of Brain Science, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Masahiko TomiyamaDepartment of Neurology, Institute of Brain Science, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Hirosaki University · JPNational Hospital Organization · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIt remains unclear why patients with young-onset Parkinson's disease more often develop levo-dihydroxyphenylalanine (L-dopa)-induced dyskinesia (LID) and have a more severe form than patients with old-onset Parkinson's disease. Previous studies using animal models have failed to show young-onset Parkinson's disease enhances LID.

objectivesTo evaluate the association of age at dopaminergic denervation (onset age) and initiation of L-dopa treatment (treatment age) with LID development in model rats.

methodsWe established rat models of young- and old-lesioned Parkinson's disease (6-hydroxydopamine lesions at 10 and 88 weeks of age, respectively). Dopaminergic denervation was confirmed by the rotational behavior test using apomorphine. Rats in the young-lesioned group were allocated to either L-dopa treatment at a young or old age, or saline treatment. Rats in the old-lesioned group were allocated to either L-dopa treatment or saline group. We evaluated L-dopa-induced abnormal involuntary movements during the 14-day treatment period. We also examined preprodynorphin mRNA expression in the striatum (a neurochemical hallmark of LID) and the volume of the medial globus pallidus (a pathological hallmark of LID).

resultsLID-like behavior was enhanced in L-dopa-treated young-lesioned rats compared with L-dopa-treated old-lesioned rats. Preprodynorphin mRNA expression was higher in L-dopa-treated young-lesioned rats than in in L-dopa-treated old-lesioned rats. The volume of the medial globus pallidus was greater in L-dopa-treated young-lesioned rats than in L-dopa-treated old-lesioned rats. Treatment age did not affect LID-like behavior or the degree of medial globus pallidus hypertrophy in the young-lesioned model.

conclusionBoth dopaminergic denervation and L-dopa initiation at a young age contributed to the development of LID; however, the former may be a more important factor.

Indexed as

6-hydroxydopamine (6-OHDA)abnormal involuntary movementdynorphinmedial globus pallidusyoung-onset Parkinson’s disease

Identifiers

PMID34054505
PMCPMC8155371
OpenAlexW3162166152

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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.