ReviewCellular and molecular life sciences : CMLS2015
Molecular imaging of levodopa-induced dyskinesias.
Review in Cellular and molecular life sciences : CMLS, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.
- A systematic review of lessons learned from PET molecular imaging research in atypical parkinsonism.European journal of nuclear medicine and molecular imaging · 2016Pooled it
- The role of neuroimaging in Parkinson's disease.Journal of neurochemistry · 2021Review
- The serotonergic system in Parkinson's patients with dyskinesia: evidence from imaging studies.Journal of neural transmission (Vienna, Austria : 1996) · 2018Review
- The Place of PET to Assess New Therapeutic Effectiveness in Neurodegenerative Diseases.Contrast media & molecular imaging · 2018Review
- PET Molecular Imaging Research of Levodopa-Induced Dyskinesias in Parkinson's Disease.Current neurology and neuroscience reports · 2017Review
- Motor Complications of Dopaminergic Medications in Parkinson's Disease.Seminars in neurology · 2017Review
- Antidyskinetic Treatment with MTEP Affects Multiple Molecular Pathways in the Parkinsonian Striatum.Parkinson's disease · 2017Article
- Chronic exposure to dopamine agonists affects the integrity of striatal DNeuroImage. Clinical · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Levodopa-induced dyskinesias (LIDs) occur in the majority of patients with Parkinson's disease (PD) following years of levodopa treatment. The pathophysiology underlying LIDs in PD is poorly understood, and current treatments generate only minor benefits for the patients. Studies with positron emission tomography (PET) molecular imaging have demonstrated that in advanced PD patients, levodopa administration induces sharp increases in striatal dopamine levels, which correlate with LIDs severity. Fluctuations in striatal dopamine levels could be the result of the attenuated buffering ability in the dopaminergically denervated striatum. Lines of evidence from PET studies indicate that serotonergic terminals could also be responsible for the development of LIDs in PD by aberrantly processing exogenous levodopa and by releasing dopamine in a dysregulated manner from the serotonergic terminals. Additionally, other downstream mechanisms involving glutamatergic, cannabinoid, opioid, cholinergic, adenosinergic, and noradrenergic systems may contribute in the development of LIDs. In this article, we review the findings from preclinical, clinical, and molecular imaging studies, which have contributed to our understanding the pathophysiology of LIDs in PD.
Indexed as
Identifiers
What OpenQuestion holds
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.