GIP has neuroprotective effects in Alzheimer and Parkinson’s disease models

Peptides ◽  
2020 ◽  
Vol 125 ◽  
pp. 170184 ◽  
Author(s):  
Zhen Qiang Zhang ◽  
Christian Hölscher
2010 ◽  
Vol 48 (8-9) ◽  
pp. 2037-2044 ◽  
Author(s):  
Mi Sun Ju ◽  
Hyo Geun Kim ◽  
Jin Gyu Choi ◽  
Jong Hoon Ryu ◽  
Jinyoung Hur ◽  
...  

RSC Advances ◽  
2016 ◽  
Vol 6 (75) ◽  
pp. 71328-71337 ◽  
Author(s):  
Bao Wang ◽  
Xing-qin Wang ◽  
Shao-song Yang ◽  
Xi Liu ◽  
Da-yun Feng ◽  
...  

In this work we found that nitidine could significantly suppress microglial activationviathe Jak2–Stat3 pathway and obviously improve behavioural function in Parkinson's disease (PD) animal models, which sheds light on PD treatment.


Author(s):  
Osmar Vieira Ramires Júnior ◽  
Barbara da Silva Alves ◽  
Paula Alice Bezerra Barros ◽  
Jamile Lima Rodrigues ◽  
Shana Pires Ferreira ◽  
...  

2021 ◽  
Vol 10 (1) ◽  
Author(s):  
Keya Li ◽  
Xinyue Li ◽  
Guiying Shi ◽  
Xuepei Lei ◽  
Yiying Huang ◽  
...  

AbstractAnimal models provide an opportunity to assess the optimal treatment way and the underlying mechanisms of direct clinical application of adipose-derived stem cells (ADSCs). Previous studies have evaluated the effects of primitive and induced ADSCs in animal models of Parkinson’s disease (PD). Here, eight databases were systematically searched for studies on the effects and in vivo changes caused by ADSC intervention. Quality assessment was conducted using a 10-item risk of bias tool. For the subsequent meta-analysis, study characteristics were extracted and effect sizes were computed. Ten out of 2324 published articles (n = 169 animals) were selected for further meta-analysis. After ADSC therapy, the rotation behavior (10 experiments, n = 156 animals) and rotarod performance (3 experiments, n = 54 animals) were improved (P < 0.000 01 and P = 0.000 3, respectively). The rotation behavior test reflected functional recovery, which may be due to the neurogenesis from neuronally differentiated ADSCs, resulting in a higher pooled effect size of standard mean difference (SMD) (− 2.59; 95% CI, − 3.57 to − 1.61) when compared to that of primitive cells (− 2.18; 95% CI, − 3.29 to − 1.07). Stratified analyses by different time intervals indicated that ADSC intervention exhibited a long-term effect. Following the transplantation of ADSCs, tyrosine hydroxylase-positive neurons recovered in the lesion area with pooled SMD of 13.36 [6.85, 19.86]. Transplantation of ADSCs is a therapeutic option that shows long-lasting effects in animal models of PD. The potential mechanisms of ADSCs involve neurogenesis and neuroprotective effects. The standardized induction of neural form of transplanted ADSCs can lead to a future application in clinical practice.


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