ArticleFrontiers in neuroscience2013
Perspective: Identification of genetic variants associated with dopaminergic compensatory mechanisms in early Parkinson's disease.
Article in Frontiers in neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Aging, not Parkinson's disease, decreases a recalibration of body ownership caused by vision-respiratory interaction.Frontiers in physiology · 2024Article
- Modulation of time in Parkinson's disease: a review and perspective on cognitive rehabilitation.Frontiers in psychiatry · 2024Review
- Defining the concept of reserve in the motor domain: a systematic review.Frontiers in neuroscience · 2024Review
- Article
- Dysfunctional counting of mental time in Parkinson's disease.Scientific reports · 2016Article
- The V81M variant of tyrosine hydroxylase is associated with more severe freezing of gait in Parkinson's disease.Parkinsonism & related disorders · 2016Article
- Parkin cooperates with GDNF/RET signaling to prevent dopaminergic neuron degeneration.The Journal of clinical investigation · 2015Article
- Pharmacogenetics of antipsychotic-induced movement disorders as a resource for better understanding Parkinson's disease modifier genes.Frontiers in neurology · 2015Review
- Applying imaging genetics to ADHD: the promises and the challenges.Molecular neurobiology · 2014Review
- Gene expression profiling analysis of the putamen for the investigation of compensatory mechanisms in Parkinson's disease.BMC neurology · 2013Article
- Article
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9 authors.
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Abstract
Parkinson's disease (PD) is slowly progressive, and heterogeneity of its severity among individuals may be due to endogenous mechanisms that counterbalance the striatal dopamine loss. In this perspective paper, we introduce a neuroimaging-genetic approach to identify genetic variants, which may contribute to this compensation. First, we briefly review current known potential compensatory mechanisms for premotor and early disease PD, located in the striatum and other brain regions. Then, we claim that a mismatch between mild symptomatic disease, manifested by low motor score on the Unified PD Rating Scale (UPDRS), and extensive Nigro-Striatal (NS) degeneration, manifested by reduced uptake of [(123)I]FP-CIT, is indicative of compensatory processes. If genetic variants are associated with the severity of motor symptoms, while the level of striatal terminals degeneration measured by ligand uptake is taken into account and controlled in the analysis, then these variants may be involved in functional compensatory mechanisms for striatal dopamine deficit. To demonstrate feasibility of this approach, we performed a small "proof of concept" study (candidate gene design) in a sample of 28 Jewish PD patients, and preliminary results are presented.
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