Dopa and Dopamine Cause the Destruction of Cultured Nerve Cells in the Presence of Iron: Possible Mechanism of the Nigral Degeneration in Parkinson’s Disease

Author(s):  
Makoto Tanaka ◽  
Akemi Sotomatsu ◽  
Hiroko Kanai ◽  
Shunsaku Hirai ◽  
Minoru Nakano
2020 ◽  
Vol 16 ◽  
Author(s):  
Fatma Ağin

Background: Dopamine agonists are useful drugs for the management of patients with Parkinson's disease in the early stages and in later stages of the disease. Parkinson's disease is a progressive neurodegenerative disease that primarily affects dopamine-producing nerve cells in the brain. They bind to dopamine receptors in nerve cells that regulate body movement and motor function. Electroanalytical methods are used in medicinal, clinical and pharmaceutical research. The voltammetry is one of the most commonly used electroanalytical methods. The aims of this review are to gather and discuss studies of voltammetric methods used in determination of dopamine agonists. Method: This review includes the use of various voltammetric methods for determination studies of dopamine agonists from pharmaceutical dosage forms and biological samples. These studies were examined in terms of used voltammetric method or methods, working electrode, buffer, pH and validation parameters. Results: Cabergoline, pramipexole, ropinirole have more studies, while bromocriptine and apomorphine have fewer studies in the literature. Differential pulse voltammetry and square wave voltammetry methods were the most applied methods for determination of dopamine agonist drugs from pharmaceuticals and biological samples. But, stripping, cyclic and lineer sweep voltammetry methods are less applied methods. In this studies, a lot of modified electrodes were developed and used to analyse of dopamine agonists. Conclusion: The voltammetric methods supply determination of therapeutic agents and/or their metabolites in clinical samples at extremely low concentrations without the necessity for the sample pre-treatment or time consuming extraction steps. Also the modified electrodes and validated voltammetric methods provide good stability, repeatability, reproducibility and high recovery for the analysis of the analyte.


2017 ◽  
Vol 38 (5) ◽  
pp. 2627-2634 ◽  
Author(s):  
Daniel E. Huddleston ◽  
Jason Langley ◽  
Jan Sedlacik ◽  
Kai Boelmans ◽  
Stewart A. Factor ◽  
...  

2021 ◽  
Vol 22 (18) ◽  
pp. 10161
Author(s):  
Tapan Behl ◽  
Piyush Madaan ◽  
Aayush Sehgal ◽  
Sukhbir Singh ◽  
Neelam Sharma ◽  
...  

One of the utmost frequently emerging neurodegenerative diseases, Parkinson’s disease (PD) must be comprehended through the forfeit of dopamine (DA)-generating nerve cells in the substantia nigra pars compacta (SN-PC). The etiology and pathogenesis underlying the emergence of PD is still obscure. However, expanding corroboration encourages the involvement of genetic and environmental factors in the etiology of PD. The destruction of numerous cellular components, namely oxidative stress, ubiquitin-proteasome system (UPS) dysfunction, autophagy-lysosome system dysfunction, neuroinflammation and programmed cell death, and mitochondrial dysfunction partake in the pathogenesis of PD. Present-day pharmacotherapy can alleviate the manifestations, but no therapy has been demonstrated to cease disease progression. Peroxisome proliferator-activated receptors (PPARs) are ligand-directed transcription factors pertaining to the class of nuclear hormone receptors (NHR), and are implicated in the modulation of mitochondrial operation, inflammation, wound healing, redox equilibrium, and metabolism of blood sugar and lipids. Numerous PPAR agonists have been recognized to safeguard nerve cells from oxidative destruction, inflammation, and programmed cell death in PD and other neurodegenerative diseases. Additionally, various investigations suggest that regular administration of PPAR-activating non-steroidal anti-inflammatory drugs (NSAIDs) (ibuprofen, indomethacin), and leukotriene receptor antagonists (montelukast) were related to the de-escalated evolution of neurodegenerative diseases. The present review elucidates the emerging evidence enlightening the neuroprotective outcomes of PPAR agonists in in vivo and in vitro models experiencing PD. Existing articles up to the present were procured through PubMed, MEDLINE, etc., utilizing specific keywords spotlighted in this review. Furthermore, the authors aim to provide insight into the neuroprotective actions of PPAR agonists by outlining the pharmacological mechanism. As a conclusion, PPAR agonists exhibit neuroprotection through modulating the expression of a group of genes implicated in cellular survival pathways, and may be a propitious target in the therapy of incapacitating neurodegenerative diseases like PD.


2015 ◽  
Vol 87 (6) ◽  
pp. 633-641 ◽  
Author(s):  
Helen Ling ◽  
Seamus Kearney ◽  
Helen Lai Kuen Yip ◽  
Laura Silveira-Moriyama ◽  
Tamas Revesz ◽  
...  

2021 ◽  
Vol 11 (12) ◽  
pp. 1573
Author(s):  
Samay Prakash ◽  
Wayne G. Carter

Currently, there are no pharmacological treatments able to reverse nigral degeneration in Parkinson’s disease (PD), hence the unmet need for the provision of neuroprotective agents. Cannabis-derived phytocannabinoids (CDCs) and resveratrol (RSV) may be useful neuroprotective agents for PD due to their anti-oxidative and anti-inflammatory properties. To evaluate this, we undertook a systematic review of the scientific literature to assess the neuroprotective effects of CDCs and RSV treatments in pre-clinical in vivo animal models of PD. The literature databases MEDLINE, EMBASE, PsychINFO, PubMed, and Web of Science core collection were systematically searched to cover relevant studies. A total of 1034 publications were analyzed, of which 18 met the eligibility criteria for this review. Collectively, the majority of PD rodent studies demonstrated that treatment with CDCs or RSV produced a significant improvement in motor function and mitigated the loss of dopaminergic neurons. Biochemical analysis of rodent brain tissue suggested that neuroprotection was mediated by anti-oxidative, anti-inflammatory, and anti-apoptotic mechanisms. This review highlights the neuroprotective potential of CDCs and RSV for in vivo models of PD and therefore suggests their potential translation to human clinical trials to either ameliorate PD progression and/or be implemented as a prophylactic means to reduce the risk of development of PD.


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