scholarly journals The role of trophic factors and inflammatory processes in physical activity-induced neuroprotection in Parkinson’s disease

2017 ◽  
Vol 71 (1) ◽  
pp. 0-0 ◽  
Author(s):  
Ewelina Pałasz ◽  
Agnieszka Bąk ◽  
Anna Gąsiorowska ◽  
Grażyna Niewiadomska
Keyword(s):  
Physical Activity ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Supportive Therapy ◽  
Trophic Factors ◽  
Moderate Physical Activity ◽  
Motor Impairments ◽  
Current State ◽  
Inflammatory Processes

Glial cells and neurotrophins play an important role in maintaining homeostasis of the CNS. Disturbances of their function can lead to a number of nervous system diseases, including Parkinson’s disease (PD). Current clinical studies provide evidence that moderate physical activity adapted to the health status of PD patients can support pharmacological treatment, slow down the onset of motor impairments, and extend the patients period of independence. Physical activity, by stimulating the production and release of endogenous trophic factors, prevents the neurodegeneration of dopaminergic neurons via inhibition of inflammatory processes and the reduction of oxidative stress. The aim of this study is to present the current state of knowledge for the anti-inflammatory and neuroprotective properties of physical activity as a supportive therapy in Parkinson’s disease.

scholarly journals Optimizing Cognitive Training for the Treatment of Cognitive Dysfunction in Parkinson’s Disease: Current Limitations and Future Directions

2021 ◽  
Vol 13 ◽  
Author(s):  
Bianca Guglietti ◽  
David Hobbs ◽  
Lyndsey E. Collins-Praino
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cognitive Dysfunction ◽  
Cognitive Training ◽  
Assistive Technologies ◽  
Motor Impairments ◽  
Future Directions ◽  
Cognitive Domains ◽  
Current State ◽  
Non Motor Symptoms

Cognitive dysfunction, primarily involving impairments in executive function, visuospatial function and memory, is one of the most common non-motor symptoms of Parkinson’s disease (PD). Currently, the only pharmacological treatments available for the treatment of cognitive dysfunction in PD provide variable benefit, making the search for potential non-pharmacological therapies to improve cognitive function of significant interest. One such therapeutic strategy may be cognitive training (CT), which involves the repetition of standardized tasks with the aim of improving specific aspects of cognition. Several studies have examined the effects of CT in individuals with PD and have shown benefits in a variety of cognitive domains, but the widespread use of CT in these individuals may be limited by motor impairments and other concerns in study design. Here, we discuss the current state of the literature on the use of CT for PD and propose recommendations for future implementation. We also explore the potential use of more recent integrative, adaptive and assistive technologies, such as virtual reality, which may optimize the delivery of CT in PD.

The key role of physical activity against the neuromuscular deterioration in patients with Parkinson’s disease

2021 ◽  
Author(s):  
Camilla Martignon ◽  
Federico Ruzzante ◽  
Gaia Giuriato ◽  
Fabio Giuseppe Laginestra ◽  
Anna Pedrinolla ◽  
...  
Keyword(s):  
Physical Activity ◽  
Parkinson’S Disease ◽  
Parkinson's Disease

scholarly journals Unilateral 6-OHDA <i>th-fgfr1</i>(<i>tk-</i>) mouse model supports the role of FGFs in Parkinson’s disease and the effects of nicotine and L-DOPA on spontaneous motor impairments

Health ◽  
2012 ◽  
Vol 04 (11) ◽  
pp. 1178-1190 ◽  
Author(s):  
Aaron Kucinski ◽  
Scott Wersinger ◽  
Ewa K. Stachowiak ◽  
Milen Radell ◽  
Renae Hesse ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Mouse Model ◽  
Motor Impairments

scholarly journals Kinin Peptides Enhance Inflammatory and Oxidative Responses Promoting Apoptosis in a Parkinson’s Disease Cellular Model

2016 ◽  
Vol 2016 ◽  
pp. 1-14 ◽  
Author(s):  
Anna Niewiarowska-Sendo ◽  
Andrzej Kozik ◽  
Ibeth Guevara-Lora
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Receptor Expression ◽  
Cellular Model ◽  
Enhanced Production ◽  
Kinin Receptors ◽  
Kinin Receptor ◽  
Inflammatory Processes

Kinin peptides ubiquitously occur in nervous tissue and participate in inflammatory processes associated with distinct neurological disorders. These substances have also been demonstrated to promote the oxidative stress. On the other hand, the importance of oxidative stress and inflammation has been emphasized in disorders that involve the neurodegenerative processes such as Parkinson’s disease (PD). A growing number of reports have demonstrated the increased expression of kinin receptors in neurodegenerative diseases. In this study, the effect of bradykinin and des-Arg10-kallidin, two representative kinin peptides, was analyzed with respect to inflammatory response and induction of oxidative stress in a PD cellular model, obtained after stimulation of differentiated SK-N-SH cells with a neurotoxin, 1-methyl-4-phenylpyridinium. Kinin peptides caused an increased cytokine release and enhanced production of reactive oxygen species and NO by cells. These changes were accompanied by a loss of cell viability and a greater activation of caspases involved in apoptosis progression. Moreover, the neurotoxin and kinin peptides altered the dopamine receptor 2 expression. Kinin receptor expression was also changed by the neurotoxin. These results suggest a mediatory role of kinin peptides in the development of neurodegeneration and may offer new possibilities for its regulation by using specific antagonists of kinin receptors.

Fetal Grafting for Parkinson's Disease: Expression of Immune Markers in Two Patients with Functional Fetal Nigral Implants

1997 ◽  
Vol 6 (3) ◽  
pp. 213-219 ◽  
Author(s):  
Jeffrey H. Kordower ◽  
Scot Styren ◽  
Martha Clarke ◽  
Stephen T. Dekosky ◽  
C. Warren Olanow ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Immune System ◽  
Immune Cells ◽  
Trophic Factors ◽  
Immune Markers ◽  
Open Label ◽  
Hla Dr ◽  
And Function

In a number of centers throughout the world, fetal nigral transplantation is being performed for the treatment of Parkinson's disease (PD). Clinical results have been inconsistent. One parameter that differs among transplant studies is the degree and manner by which patients are immunosuppressed following transplantation. Indeed, the role of the immune system following fetal grafting in humans is not well understood. Recently, two patients from our open label trial that received fetal nigral implants have come to autopsy. These patients were immunosuppressed with cyclosporin for 6 mo posttransplantation and survived for a total of 18 mo postgrafting. Robust survival of grafted dopamine-containing cells was observed in both cases. Immunostaining for HLA-DR revealed a dense collection of cells within grafts from both cases. HLA-DR staining was rarely observed within the host including non-grafted regions of the striatum. A more detailed analysis of immune markers was performed in Case 2. Numerous pan macrophages, T-cells, and B-cells were observed within graft sites located in the postcommissural putamen. In contrast, staining for these immune cells was not observed within the ungrafted anterior putamen. These findings suggest that even in healthy appearing functional nigral implants, grafts are invaded by host immune cells that could compromise their long-term viability and function. Alternatively, immune cells are known to secrete trophic factors, which may ultimately favor graft survival and function. Further work is needed to understand the role of the immune system in fetal grafting.

scholarly journals A Case-Control Association Study of RANTES (-28C>G) Polymorphism as a Risk Factor for Parkinson’s Disease in Isparta, Turkey

2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Nilufer Sahin-Calapoglu ◽  
Serpil Demirci ◽  
Mustafa Calapoglu ◽  
Baris Yasar
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Association Study ◽  
Chemokine Receptors ◽  
Case Control ◽  
Pcr Rflp ◽  
Genes Encoding ◽  
Inflammatory Processes ◽  
Control Association

Background. Recent studies have revealed that inflammatory processes are involved in the pathogenesis of Parkinson’s disease (PD). Multiple lines of evidence have suggested that chemokines and their receptors are involved in several neurodegenerative disorders. We have examined whether genetic polymorphisms at the genes encoding chemokines IL-8 (-251A>T), MCP-1 (-2518A/G), and RANTES (-28C>G) and chemokine receptors CCR2 (V64I) and CCR5 (-Δ32) were associated with sporadic PD risk in Isparta, Turkey. Method. The pilot case-control association study included 30 PD patients and 60 control subjects, who were all genotyped with PCR-RFLP for the five polymorphisms. Their genotype and haplotype frequencies were compared statistically. Results. One SNP (-28C>G) in RANTES revealed a significant association with PD (P (allele) < 0.0001, p-trend = 0.0007). The risk allele (G) in the homozygous and dominant models (OR = 17.29 and 32.10, 95% CI = 0.86–347.24 and 1.74–591.937, resp.) suggests additional PD risk. The haplotype TGCAN from the IL-8 (-251A>T), MCP-1 (-2518A>G), RANTES (-28C>G), CCR-2 (V64I), and CCR-5 (-Δ32) has protective effect (OR = 0.08 [CI = 0.01–0.63], p=0.019). Conclusions. Our data are the first indication of the role of RANTES (-28C>G) in PD risk.

scholarly journals The role of selected antioxidants in the development and treatment of Parkinson’s disease

2019 ◽  
Vol 73 ◽  
pp. 516-528
Author(s):  
Dominika Markowska ◽  
Daria Malicka ◽  
Jarosław Nuszkiewicz ◽  
Karolina Szewczyk-Golec
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Modern Medicine ◽  
Substantia Nigra Pars Compacta ◽  
Current State ◽  
And Oxidative Stress ◽  
Significant Health

The widespread aging of societies results in the intensification of the development of neurodegenerative diseases associated with advanced age, including Parkinson’s disease. Unfortunately, modern medicine is not able to unequivocally determine the etiopathogenesis of the disease, which is why no causative treatment can be given. According to the current state of knowledge, in the course of Parkinson’s disease the substantia nigra pars compacta in the midbrain degenerates, leading to a decrease in dopamine levels in the patient’s brain. This results in neurotransmission disturbances and the development of undesirable effects. Neurodegenerative changes are supposedly caused by the combination of various factors, including genetic factors, chronic inflammation, the interaction of toxins, disturbances in protein metabolism, and oxidative stress. The therapeutic possibilities associated with the administration of antioxidants, which could alleviate increased oxidative stress and contribute to the better quality of life of the patient, are considered. Taking into account the studies on numerous antioxidants, such as coenzyme Q10, B vitamins, vitamin D, vitamin E and resveratrol, it cannot be unequivocally stated that this is an effective treatment, because experiments carried out on both humans and animals gave conflicting results. It is reasonable to say that antioxidant deficiencies should be avoided and the physiological levels should be sought, as this may be translated into significant health benefits.

scholarly journals Inflammatory Mechanisms of Neurodegeneration in Toxin-Based Models of Parkinson's Disease

2011 ◽  
Vol 2011 ◽  
pp. 1-18 ◽  
Author(s):  
Darcy Litteljohn ◽  
Emily Mangano ◽  
Melanie Clarke ◽  
Jessica Bobyn ◽  
Kerry Moloney ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Proinflammatory Cytokines ◽  
Inflammatory Factors ◽  
Toxin Exposure ◽  
Environmental Agents ◽  
Inflammatory Processes ◽  
Midbrain Dopamine ◽  
Necrosis Factor

Parkinson's disease (PD) has been associated with exposure to a variety of environmental agents, including pesticides, heavy metals, and organic pollutants; and inflammatory processes appear to constitute a common mechanistic link among these insults. Indeed, toxin exposure has been repeatedly demonstrated to induce the release of oxidative and inflammatory factors from immunocompetent microglia, leading to damage and death of midbrain dopamine (DA) neurons. In particular, proinflammatory cytokines such as tumor necrosis factor-αand interferon-γ, which are produced locally within the brain by microglia, have been implicated in the loss of DA neurons in toxin-based models of PD; and mounting evidence suggests a contributory role of the inflammatory enzyme, cyclooxygenase-2. Likewise, immune-activating bacterial and viral agents were reported to have neurodegenerative effects themselves and to augment the deleterious impact of chemical toxins upon DA neurons. The present paper will focus upon the evidence linking microglia and their inflammatory processes to the death of DA neurons following toxin exposure. Particular attention will be devoted to the possibility that environmental toxins can activate microglia, resulting in these cells adopting a “sensitized” state that favors the production of proinflammatory cytokines and damaging oxidative radicals.

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