scholarly journals Disease Progression-Dependent Expression of CD200R1 and CX3CR1 in Mouse Models of Parkinson’s Disease

2020 ◽  
Vol 11 (2) ◽  
pp. 254 ◽  
Author(s):  
Le Wang ◽  
Yang Liu ◽  
Shuxin Yan ◽  
Tianshu Du ◽  
Xia Fu ◽  
...  
2021 ◽  
Vol 81 ◽  
pp. 307-311 ◽  
Author(s):  
Claudio Liguori ◽  
Valentino De Franco ◽  
Rocco Cerroni ◽  
Matteo Spanetta ◽  
Nicola Biagio Mercuri ◽  
...  

2021 ◽  
Author(s):  
Ecehan Abdik ◽  
Tunahan Cakir

Genome-scale metabolic networks enable systemic investigation of metabolic alterations caused by diseases by providing interpretation of omics data. Although Mus musculus (mouse) is one of the most commonly used model...


2012 ◽  
Vol 18 (6) ◽  
pp. 942-951 ◽  
Author(s):  
Alison C. Simioni ◽  
Alain Dagher ◽  
Lesley K. Fellows

AbstractConverging evidence, including observations in patients with Parkinson's disease (PD), suggests that dopamine plays a role in impulsivity. This multi-faceted construct includes considerations of both time and risk; determining how these more specific processes are affected by PD and dopaminergic treatment can inform neurobiological models. We examined the effects of PD and its treatment on temporal discounting and risky decision-making in a cohort of 23 mild-moderate PD patients and 20 healthy participants. Patients completed the Balloon Analogue Risk Task and a temporal discounting paradigm both on and off their usual dopamine replacement therapy. PD patients did not differ from controls in their initial risk-taking on the Balloon Analogue Risk Task, but took progressively more risks across trials when on medication. A subset of patients and controls was tested again, 1.5–3 years later, to explore the effects of disease progression. On follow-up, baseline risk-taking diminished in patients, but the tendency to take increasing risks across trials persisted. Neither disease progression nor its treatment affected the temporal discounting rate. These findings suggest a different neural basis for temporal discounting and risk-taking, and demonstrate that risk-taking can be further decomposed into initial and trial-by-trial effects, with dopamine affecting only the latter. (JINS, 2012, 18, 1–10)


The neurodegenerative disorder is a prolonged persistence curse and effect on economic and physical challenges in an aging world. Parkinson has come in the second category of disability disorders and associated with progressive dopaminergic neuronal degeneration with severe motor complications. It is an observation that gradual disease progression causes 70% degeneration of striatal dopaminergic neurons. Globally there are around 7-10 million patients with Parkinson's disease, however, there are huge efforts for therapeutic improvement. According to studies, no single molecular pathway was pointed out as a single etiology to control disease progression due to a lack of targeted therapeutic strategies. Previously implemented symptomatic treatments include L-dopa (L-3,4-dihydroxyphenylalanine), deep brain stimulation, and the surgical insertion of a medical device. This leads to dyskinesia, dystonia and a higher risk of major surgical complications respectively. However, not all the above-mentioned therapies cannot regenerate the dopaminergic neurons in Parkinson’s disease patients. Recent advances in the field of cellular therapy have shown promising outcomes by differentiation of multipotent mesenchymal stem cells into dopaminergic neurons under the influence of a regenerative substance. In this review, we have discussed the differentiation of dopaminergic neurons by using different cell types that can be used as a cellular therapeutic approach for Parkinson’s disease. The information was collected through a comprehensive search using the keywords, “Parkinson Disease, Dopamine, Brain derived neurotrophic factor and neuron from reliable search engines, PubMed, Google Scholar and Medline reviews from the year 2010 to 2020.


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