A microfiber scaffold-based 3D in vitro human neuronal culture model of Alzheimer's disease

2020 ◽  
Vol 8 (17) ◽  
pp. 4861-4874
Author(s):  
Vivek Damodar Ranjan ◽  
Lifeng Qiu ◽  
Jolene Wei-Ling Lee ◽  
Xuelong Chen ◽  
Se Eun Jang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Amyloid Beta ◽  
Neuronal Culture ◽  
Neurogenic Differentiation ◽  
Highly Efficient ◽  
Model Of Alzheimer’S Disease ◽  
Culture Model ◽  
Amyloid Beta 42 ◽  
Tau Expression

Highly efficient neurogenic differentiation, maturation as well as spontaneous amplification of pathogenic amyloid-beta 42 (Aβ42) and phospho-tau expression were achieved on interfacing iPSC-derived neurons with 3D PLGA microfiber scaffolds.

P3-322 Altered expression of synaptic and immediate early genes in a neuronal culture model of Alzheimer's disease

2004 ◽  
Vol 25 ◽  
pp. S446-S447
Author(s):  
Davide Tampellini ◽  
Claudia G. Almeida ◽  
Eric M. Snyder ◽  
Reisuke H. Takahashi ◽  
Giovanni Manfredi ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Immediate Early Genes ◽  
Neuronal Culture ◽  
Immediate Early ◽  
Altered Expression ◽  
Early Genes ◽  
Model Of Alzheimer’S Disease ◽  
Culture Model

Oxymatrine attenuates amyloid beta 42 (Aβ1–42)-induced neurotoxicity in primary neuronal cells and memory impairment in rats

2019 ◽  
Vol 97 (2) ◽  
pp. 99-106 ◽  
Author(s):  
Peiliang Dong ◽  
Xiaomeng Ji ◽  
Wei Han ◽  
Hua Han
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Beta ◽  
Neuronal Cells ◽  
Morris Water Maze Test ◽  
Dependent Manner ◽  
Amyloid Beta 42

Amyloid beta 42 (Aβ1–42)-induced oxidative stress causes the death of neuronal cells and is involved in the development of Alzheimer’s disease. Oxymatrine (OMT) inhibits oxidative stress. In this study, we investigated the effect of OMT on Aβ1–42-induced neurotoxicity in vivo and in vitro. In the Morris water maze test, OMT significantly decreased escape latency and increased the number of platform crossings. In vitro, OMT markedly increased cell viability and superoxide dismutase activity. Moreover, OMT decreased lactate dehydrogenase leakage, malondialdehyde content, and reactive oxygen species in a dose-dependent manner. OMT upregulated the ratio of Bcl-2/Bax and downregulated the level of caspase-3. Furthermore, OMT inhibited the activation of MAP kinase (ERK 1/2, JNK) and nuclear factor κB. In summary, OMT may potentially be used in the treatment of Alzheimer’s disease.

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