scholarly journals The Preclinical Research Progress of Stem Cells Therapy in Parkinson’s Disease

2016 ◽  
Vol 2016 ◽  
pp. 1-6 ◽  
Author(s):  
Jun Zhang ◽  
Xianyun Wang ◽  
Jing Li ◽  
Rui Huang ◽  
Xuerui Yu ◽  
...  

Parkinson’s disease (PD) is a type of degenerative disorder of the basal ganglia, causing tremor at rest, muscle rigidity hypokinesia, and dementia. The effectiveness of drug treatments gradually diminishes because the conversion to dopamine within the brain is increasingly disrupted by the progressive degeneration of the dopaminergic terminals. After long-term treatment, most patients with PD suffer from disability that cannot be satisfactorily controlled. To solve these issues, stem cells have recently been used for cell therapy of PD. In this review, the characteristics of different stem cells and their therapeutic effects on PD treatment will be discussed.

2007 ◽  
Vol 22 (8) ◽  
pp. 1093-1096 ◽  
Author(s):  
Alexandre Berney ◽  
Michel Panisset ◽  
Abbas F. Sadikot ◽  
Alain Ptito ◽  
Alain Dagher ◽  
...  

2016 ◽  
Vol 10 (1) ◽  
pp. 42-58 ◽  
Author(s):  
Mohsin H.K. Roshan ◽  
Amos Tambo ◽  
Nikolai P. Pace

Parkinson’s disease [PD] is the second most common neurodegenerative disorder after Alzheimer’s disease, affecting 1% of the population over the age of 55. The underlying neuropathology seen in PD is characterised by progressive loss of dopaminergic neurons in the substantia nigra pars compacta with the presence of Lewy bodies. The Lewy bodies are composed of aggregates of α-synuclein. The motor manifestations of PD include a resting tremor, bradykinesia, and muscle rigidity. Currently there is no cure for PD and motor symptoms are treated with a number of drugs including levodopa [L-dopa]. These drugs do not delay progression of the disease and often provide only temporary relief. Their use is often accompanied by severe adverse effects. Emerging evidence from bothin vivoandin vitrostudies suggests that caffeine may reduce parkinsonian motor symptoms by antagonising the adenosine A2Areceptor, which is predominately expressed in the basal ganglia. It is hypothesised that caffeine may increase the excitatory activity in local areas by inhibiting the astrocytic inflammatory processes but evidence remains inconclusive. In addition, the co-administration of caffeine with currently available PD drugs helps to reduce drug tolerance, suggesting that caffeine may be used as an adjuvant in treating PD. In conclusion, caffeine may have a wide range of therapeutic effects which are yet to be explored, and therefore warrants further investigation in randomized clinical trials.


2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Sicong Li ◽  
Xu Sun ◽  
Lei Bi ◽  
Yujia Tong ◽  
Xin Liu

Parkinson’s disease (PD) is a common neurodegenerative disease in middle-aged and older adults. Abnormal proteins such as α-synuclein are essential factors in PD’s pathogenesis. Autophagy is the main participant in the clearance of abnormal proteins. The overactive or low function of autophagy leads to autophagy stress. Not only is it difficult to clear abnormal proteins but also it can cause damage to neurons. In this article, the effects of natural products ingredients, such as salidroside, paeoniflorin, curcumin, resveratrol, corynoxine, and baicalein, on regulating autophagy and protecting neurons were discussed in detail to provide a reference for the research and development of drugs for the treatment of PD.


2008 ◽  
Vol 9 (2) ◽  
pp. 115-119
Author(s):  
Viola Sacchi

Parkinson’s disease (PD) is a neurodegenerative disorder secondary to the progressive loss of dopaminergic neurons in the substantia nigra (a portion of the midbrain responsible for movement initiation and coordination) and appearance of bradykinesia, resting tremor, rigidity and postural reflex impairment. The most common symptomatic therapy is levodopa, a dopamine precursor; however, long-term treatment leads to involuntary movements and response fluctuations which add to the complexities of later disease-management. Monotherapy with dopamine agonists may represent an alternative approach with a reduced likelihood of motor complications; these drugs, initially introduced as adjunctive therapy to levodopa, are less effective in controlling motor disability and tend to cause more sideeffects than levodopa itself.


Neurology ◽  
1998 ◽  
Vol 50 (Issue 5, Supplement 5) ◽  
pp. S39-S45 ◽  
Author(s):  
C. H. Waters ◽  
M. Kurth ◽  
P. Bailey ◽  
L. M. Shulman ◽  
P. LeWitt ◽  
...  

2021 ◽  
Author(s):  
Changlin Lian ◽  
Qiongzhen Huang ◽  
Xiangyang Zhong ◽  
Zhenyan He ◽  
Boyang Liu ◽  
...  

Abstract Background Adipose-derived human mesenchymal stem cells (hADSCs) transplantation has recently emerged as a promising method in the treatment of Parkinson's disease (PD), however, the mechanism underlying has not been fully illustrated. Methods In this study, the therapeutic effects of the striatum stereotaxic injected hADSCs in 6-OHDA-induced mouse model were evaluated. Furthermore, an in vitro model of PD was constructed using tissue-organized brain slices. And the therapeutic effect was evaluated by co-culture of hADSCs and 6-OHDA-constructed brain slice. Within the analysis of hADSCs' exocrine proteins through RNA-seq, Human protein cytokine arrays and label-free quantitative proteomics, key extracellular factors were identified in hADSCs secretion environment.The degeneration of DA neurons and apoptosis were measured in PD samples in vivo and vitro models, and the beneficial effects were evaluated through quantitative reverse transcription polymerase chain reaction (qRT-PCR), western blot,Fluoro-Jade C, Tunel assay and immunofluorescence analysis. Results In this study, we discovered that hADSCs protected the dopaminergic (DA) neurons in vivo and vitro models.we identified Pentraxin3 (PTX3) as a key extracellular factor in hADSCs secretion environment. Moreover, we found that human recombinant Pentraxin3 (rhPTX3) treatment could rescue the physiological behaviour of the PD mice in-vivo, as well as prevent DA neurons from death and increase the neuronal terminals in the Ventral tegmental area (VTA) + substantia nigra pars compacta (SNc) and striatum (STR) on the PD brain slices in-vitro. Furthermore, within testing on the pro-apoptotic markers of PD mice brain following the treatment of rhPTX3, we found that rhPTX3 can prevent the apoptosis and the degeneration of DA neurons. Conclusions Overall, the current study investigated that PTX3, a hADSCs secreted protein, played a potential role in protecting the DA neurons from apoptosis and degeneration in PD progression as well as improving the motor performances in PD mice to give a possible mechanism of how hADSCs works in the cell replacement therapy in PD. Importantly, our study also provided potential translational implications for the development of PTX3-based therapeutics in PD.


Author(s):  
Donald B. Calne ◽  
Keith Burton ◽  
Jeff Beckman ◽  
W.R. Wayne Martin

ABSTRACTDopamine agonists have yielded two important advances to our understanding of the basal ganglia – they have facilitated the subdivision of different classes of dopamine receptors, and they have established the fact that important dopaminergic effects can be achieved by activation of dopamine receptors in a manner that is unrelated to anoxal impulse traffic in dopaminergic neurons – a phenomenon similar in its diffuse, slow, characteristics to an endocrine effect.The tangible clinical benefit of dopamine agonists has been evident in patients with prominent dyskinesia or wearing off reactions. It is possible that earlier use of agonists, in low doses combined with similarly low doses of levodopa, may improve the long term treatment of Parkinson’s disease, but as yet there is no firm evidence.In the future, we can expect to see agonists with more prolonged effects, deriving from the formation of active metabolites. We can also hope to gain further insight into the correlations between the various animal models of dopaminomimetic activity, and specific aspects of drug efficacy and toxicity in parkinsonian patients. Such information should allow the design of improved pharmacotherapy.


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