ReviewMovement disorders : official journal of the Movement Disorder Society2016
How compensation breaks down in Parkinson's disease: Insights from modeling of denervated striatum.
Review in Movement disorders : official journal of the Movement Disorder Society, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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
13 citing papers in PubMed.
- Time perception in cerebellar and basal ganglia stroke patients.Scientific reports · 2025Article
- First steps matter: gait initiation reveals emotion-driven motor compensation in Parkinson's disease.Brain communications · 2025Article
- Understanding the progression of Parkinson's disease: a review.BMJ neurology open · 2025Review
- Multimodal striatal neuromarkers in distinguishing parkinsonian variant of multiple system atrophy from idiopathic Parkinson's disease.CNS neuroscience & therapeutics · 2022Article
- Dopamine D3 Receptor Plasticity in Parkinson's Disease and L-DOPA-Induced Dyskinesia.Biomedicines · 2021Review
- Behavioral Tests in Neurotoxin-Induced Animal Models of Parkinson's Disease.Antioxidants (Basel, Switzerland) · 2020Review
- Dysarthria enhancement mechanism under external clear speech instruction in Parkinson's disease, progressive supranuclear palsy and multiple system atrophy.Journal of neural transmission (Vienna, Austria : 1996) · 2020Article
- A Multi-Scale Computational Model of Excitotoxic Loss of Dopaminergic Cells in Parkinson's Disease.Frontiers in neuroinformatics · 2020Article
- Compensatory dopaminergic-cholinergic interactions in conflict processing: Evidence from patients with Parkinson's disease.NeuroImage · 2019Article
- Insights into Parkinson's disease from computational models of the basal ganglia.Journal of neurology, neurosurgery, and psychiatry · 2018Review
- Conditioning Against the Pathology of Parkinson's disease.Conditioning medicine · 2018Article
- New Therapeutics to Modulate Mitochondrial Function in Neurodegenerative Disorders.Current pharmaceutical design · 2017Review
- Enhancing and Extending Biological Performance and Resilience.Dose-response : a publication of International Hormesis SocietyReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The bradykinesia and other motor signs of Parkinson's disease (PD) are linked to progressive loss of substantia nigra dopamine (DA) neurons innervating the striatum. However, the emergence of idiopathic PD is likely preceded by a prolonged subclinical phase, which may be masked by a variety of pre- and postsynaptic compensatory mechanisms. It is often considered self-evident that the signs of PD manifest only when nigrostriatal degeneration has proceeded to such an extent that putative compensatory mechanisms fail to accommodate the depletion of striatal DA levels. However, the precise nature of the compensatory mechanisms, and the reason for their ultimate failure, has been elusive. In a recent computational study we modeled the effects of progressive denervation, including changes in the dynamics of interstitial DA and also adaptive or compensatory changes in postsynaptic responsiveness to DA signaling in the course of progressive nigrostriatal degeneration. In particular, we found that failure of DA signaling can occur by different mechanisms at different disease stages. We review these results and discuss their relevance for clinical and translational research, and we draw a number of predictions from our model that might be tested in preclinical experiments.
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.