scholarly journals Clinical Utility of Opicapone in the Management of Parkinson’s Disease: A Short Review on Emerging Data and Place in Therapy

2021 ◽  
Vol Volume 11 ◽  
pp. 29-40
Author(s):  
Linda Azevedo Kauppila ◽  
Daniela Pimenta Silva ◽  
Joaquim J Ferreira
2016 ◽  
Vol 52 (1) ◽  
pp. 35-51 ◽  
Author(s):  
Michael W. Jakowec ◽  
Zhou Wang ◽  
Daniel Holschneider ◽  
Jeff Beeler ◽  
Giselle M. Petzinger

AbstractExercise and physical activity are fundamental components of a lifestyle essential in maintaining a healthy brain. This is primarily due to the fact that the adult brain maintains a high degree of plasticity and activity is essential for homeostasis throughout life. Plasticity is not lost even in the context of a neurodegenerative disorder, but could be maladaptive thus promoting disease onset and progression. A major breakthrough in treating brain disorders such as Parkinson’s disease is to drive neuroplasticity in a direction to improve motor and cognitive dysfunction. The purpose of this short review is to present the evidence from our laboratories that supports neuroplasticity as a potential therapeutic target in treating brain disorders. We consider that the enhancement of motor recovery in both animal models of dopamine depletion and in patients with Parkinson’s disease is optimized when cognitive circuits are engaged; in other words, the brain is engaged in a learning modality. Therefore, we propose that to be effective in treating Parkinson’s disease, physical therapy must employ both skill-based exercise (to drive specific circuits) and aerobic exercise (to drive the expression of molecules required to strengthen synaptic connections) components to select those neuronal circuits, such as the corticostriatal pathway, necessary to restore proper motor and cognitive behaviors. In the wide spectrum of different forms of exercise, learning as the fundamental modality likely links interventions used to treat patients with Parkinson’s disease and may be necessary to drive beneficial neuroplasticity resulting in symptomatic improvement and possible disease modification.


1995 ◽  
Vol 10 (1) ◽  
pp. 37-43 ◽  
Author(s):  
Stephen T. Gancher ◽  
John G. Nutt ◽  
William R. Woodward

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Rie Haga ◽  
Kazuhiro Sugimoto ◽  
Haruo Nishijima ◽  
Yasuo Miki ◽  
Chieko Suzuki ◽  
...  

Background. It is often difficult to differentiate Parkinson’s disease (PD) from multiple system atrophy (MSA), especially in their early stages.Objectives. To examine the clinical utility of histopathological analysis of biopsied skin from the chest wall and/or leg in differentiating between the two diseases.Methods. Skin biopsies from the lower leg and/or anterior chest wall were obtained from 38 patients with idiopathic PD (26 treated with levodopa and 12 levodopa-naïve) and 13 age-matched patients with MSA. We sought aggregates of phosphorylatedα-synuclein on cutaneous nerve fibers using double fluorescence immunohistochemistry and confocal microscopy and measured intraepidermal nerve fiber density (IENFD).Results. Phosphorylatedα-synuclein aggregates were identified on cutaneous nerves in two patients with PD (5.3%) but in none of the patients with MSA, and IENFD was significantly lower in patients with PD when compared to those with MSA. There was no difference in IENFD between levodopa-treated and levodopa-naïve patients with PD.Conclusions. Our findings suggest that an assessment of IENFD in biopsied skin could be a useful means of differentiating between PD and MSA but that detection ofα-synuclein aggregates on cutaneous nerves in the distal sites of the body is insufficiently sensitive.


2017 ◽  
Vol 28 (2) ◽  
pp. 718-726 ◽  
Author(s):  
Albert Stezin ◽  
Rajini M. Naduthota ◽  
Ragasudha Botta ◽  
Shriram Varadharajan ◽  
Abhishek Lenka ◽  
...  

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Aneesha Chauhan ◽  
Alexander F. Jeans

Parkinson’s disease (PD) is the world’s second most common neurodegenerative disease and most common movement disorder. Characterised by a loss of dopaminergic neurons and the development of intraneuronal inclusions known as Lewy bodies, it has classically been thought of as a cell-autonomous disease. However, in 2008, two groups reported the startling observation of Lewy bodies within embryonic neuronal grafts transplanted into PD patients little more than a decade previously, suggesting that PD pathology can be propagated to neighbouring cells and calling basic assumptions of our understanding of the disease into question. Subsequent research has largely served to confirm this interpretation, pointing towards a prion-like intercellular transfer of misfoldedα-synuclein, the main component of Lewy bodies, as central to PD. This shift in thinking offers a revolutionary approach to PD treatment, potentially enabling a transition from purely symptomatic therapy to direct targeting of the pathology that drives disease progression. In this short review, we appraise current experimental support for PD as a prion-like disease, whilst highlighting areas of controversy or inconsistency which must be resolved. We also offer a brief discussion of the therapeutic implications of these discoveries.


The Lancet ◽  
2011 ◽  
Vol 377 (9766) ◽  
pp. 613-614 ◽  
Author(s):  
Christine Klein ◽  
Andreas Ziegler

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