scholarly journals Computational model of precision grip in Parkinson's disease: a utility based approach

2013 ◽  
Vol 7 ◽  
Author(s):  
Ankur Gupta ◽  
Pragathi P. Balasubramani ◽  
V. Srinivasa Chakravarthy
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Computational Model ◽  
Precision Grip

scholarly journals Fine Manual Dexterity Assessment After Autologous Neural Cell Ecosystem (ANCE) Transplantation in a Non-human Primate Model of Parkinson’s Disease

2019 ◽  
Vol 33 (7) ◽  
pp. 553-567 ◽  
Author(s):  
Simon Borgognon ◽  
Jérôme Cottet ◽  
Véronique Moret ◽  
Pauline Chatagny ◽  
Laura Carrara ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Functional Recovery ◽  
Rating Scales ◽  
Precision Grip ◽  
Subjective Assessment ◽  
Neural Cell ◽  
Manual Dexterity ◽  
Primate Model ◽  
The Impact

Background. Autologous neural cell ecosystem (ANCE) transplantation improves motor recovery in MPTP monkeys. These motor symptoms were assessed using semi-quantitative clinical rating scales, widely used in many studies. However, limitations in terms of sensitivity, combined with relatively subjective assessment of their different items, make inter-study comparisons difficult to achieve. Objective. The aim of this study was to quantify the impact of MPTP intoxication in macaque monkeys on manual dexterity and assess whether ANCE can contribute to functional recovery. Methods. Four animals were trained to perform 2 manual dexterity tasks. After reaching a motor performance plateau, the animals were subjected to an MPTP lesion. After the occurrence of a spontaneous functional recovery plateau, all 4 animals were subjected to ANCE transplantation. Results. Two of 4 animals underwent a full spontaneous recovery before the ANCE transplantation, whereas the 2 other animals (symptomatic) presented moderate to severe Parkinson’s disease (PD)-like symptoms affecting manual dexterity. The time to grasp small objects using the precision grip increased in these 2 animals. After ANCE transplantation, the 2 symptomatic animals underwent a significant functional recovery, reflected by a decrease in time to execute the different tasks, as compared with the post-lesion phase. Conclusions. Manual dexterity is affected in symptomatic MPTP monkeys. The 2 manual dexterity tasks reported here as pilot are pertinent to quantify PD symptoms and reliably assess a treatment in MPTP monkeys, such as the present ANCE transplantation, to be confirmed in a larger cohort of animals before future clinical applications.

scholarly journals Precision grip and Parkinson's disease

Brain ◽  
1998 ◽  
Vol 121 (9) ◽  
pp. 1771-1784 ◽  
Author(s):  
S. Fellows
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Precision Grip

scholarly journals A Computational Model of Levodopa-Induced Toxicity in Substantia Nigra Pars Compacta in Parkinson’s Disease

2020 ◽  
Author(s):  
Vignayanandam Ravindernath Muddapu ◽  
Karthik Vijayakumar ◽  
Keerthiga Ramakrishnan ◽  
V Srinivasa Chakravarthy
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Substantia Nigra ◽  
Computational Model ◽  
Energy Demand ◽  
High Energy ◽  
Substantia Nigra Pars Compacta ◽  
Striatal Neurons ◽  
Energy Deficiency

ABSTRACTBackgroundParkinson’s disease (PD) is caused by the progressive loss of dopaminergic cells in substantia nigra pars compacta (SNc). The root cause of this cell loss in PD is still not decisively elucidated. A recent line of thinking traces the cause of PD neurodegeneration to metabolic deficiency. Due to exceptionally high energy demand, SNc neurons exhibit a higher basal metabolic rate and higher oxygen consumption rate, which results in oxidative stress. Recently, we have suggested that the excitotoxic loss of SNc cells might be due to energy deficiency occurring at different levels of neural hierarchy. Levodopa (LDOPA), a precursor of dopamine, which is used as a symptom-relieving treatment for PD, leads to outcomes that are both positive and negative. Several researchers suggested that LDOPA might be harmful to SNc cells due to oxidative stress. The role of LDOPA in the course of PD pathogenesis is still debatable.New MethodWe hypothesize that energy deficiency can lead to LDOPA-induced toxicity (LIT) in two ways: by promoting dopamine-induced oxidative stress and by exacerbating excitotoxicity in SNc. We present a multiscale computational model of SNc-striatum system, which will help us in understanding the mechanism behind neurodegeneration postulated above and provides insights for developing disease-modifying therapeutics.ResultsIt was observed that SNc terminals are more vulnerable to energy deficiency than SNc somas. During LDOPA therapy, it was observed that higher LDOPA dosage results in increased loss of somas and terminals in SNc. It was also observed that co-administration of LDOPA and glutathione (antioxidant) evades LDOPA-induced toxicity in SNc neurons.Comparison with Existing MethodsOur proposed multiscale model of SNc-striatum system is first of its kind, where SNc neuron was modelled at biophysical level, and striatal neurons were modelled at spiking level.ConclusionsWe show that our proposed model was able to capture LDOPA-induced toxicity in SNc, caused by energy deficiency.

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