ReviewComputational and structural biotechnology journal2017
Are the Symptoms of Parkinsonism Cortical in Origin?
Review in Computational and structural biotechnology journal, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
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Who cites it
7 citing papers in PubMed, 16 citations in OpenAlex.
- Cortical Intra-Layer Hypersynchronization in Levodopa-Induced Dyskinesia Mouse Model.Brain and behavior · 2025Article
- The improved thalamo-cortical spiking network model of deep brain stimulation.Frontiers in computational neuroscience · 2025Article
- Computational analysis of two novel deep brain stimulation pulsing patterns on a thalamocortical network model of Parkinson's disease.Frontiers in network physiology · 2025Article
- Dimensionality reduction and recurrence analysis reveal hidden structures of striatal pathological states.Frontiers in systems neuroscience · 2022Article
- Early decreases in cortical mid-gamma peaks coincide with the onset of motor deficits and precede exaggerated beta build-up in rat models for Parkinson's disease.Neurobiology of disease · 2021Article
- An Introspective Approach: A Lifetime of Parkinson's Disease Research and Not Much to Show for it Yet?Cells · 2021Article
- Beyond Emotions: Oscillations of the Amygdala and Their Implications for Electrical Neuromodulation.Frontiers in neuroscience · 2019Review
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We present three reasons to suspect that the major deleterious consequence of dopamine loss from the striatum is a cortical malfunction. We suggest that it is cortex, rather than striatum, that should be considered as the source of the debilitating symptoms of Parkinson's disease (PD) since:1.Cortical synapses onto striatal dendritic spines are lost in PD.2.All known treatments of the symptoms of PD disrupt beta oscillations. Oscillations that are also disrupted following antidromic activation of cortical neurons.3.The final output of basal ganglia directly modulates thalamic connections to layer I of frontal cortical areas, regions intimately associated with motor behaviour. These three reasons combined with evidence that the current summary diagram of the basal ganglia involvement in PD is imprecise at best, suggest that a re-orientation of the treatment strategies towards cortical, rather than striatal malfunction, is overdue.
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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.