A Cell Model for the Initial Phase of Sporadic Alzheimer's Disease

2014 ◽  
Vol 42 (2) ◽  
pp. 395-411 ◽  
Author(s):  
Carola Stockburger ◽  
Vicki A.M. Gold ◽  
Thea Pallas ◽  
Natalie Kolesova ◽  
Davide Miano ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Initial Phase ◽  
Cell Model ◽  
Sporadic Alzheimer’S Disease ◽  
A Cell

Pharmacological Modulations of the Serotonergic System in a Cell-Model of Familial Alzheimer’s Disease

2016 ◽  
Vol 53 (1) ◽  
pp. 349-361 ◽  
Author(s):  
Walid Tajeddinn ◽  
Torbjörn Persson ◽  
Javier Calvo-Garrido ◽  
Mohammed Seed Ahmed ◽  
Silvia Maioli ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cell Model ◽  
Serotonergic System ◽  
Familial Alzheimer’S Disease ◽  
A Cell ◽  
Familial Alzheimer's Disease

Synthesis and approbation of new neuroprotective chemicals of pyrrolyl- and indolylazine classes in a cell model of Alzheimer's disease

2021 ◽  
pp. 113577
Author(s):  
Elizaveta A. Dutysheva ◽  
Irina A. Utepova ◽  
Maria A. Trestsova ◽  
Alexander S. Anisimov ◽  
Valery N. Charushin ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cell Model ◽  
Model Of Alzheimer’S Disease ◽  
A Cell

scholarly journals PIAS3 suppresses damage in an Alzheimer’s disease cell model by inducing the STAT3-associated STAT3/Nestin/Nrf2/HO-1 pathway

2021 ◽  
Vol 27 (1) ◽  
Author(s):  
Chen Li ◽  
Ruili Wang ◽  
Youyou Zhang ◽  
Chunting Hu ◽  
Qiaoya Ma
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cell Model ◽  
Control Group ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
A Cell ◽  
The Central Nervous System ◽  
And Oxidative Stress

Abstract Background Alzheimer’s disease (AD), the most common form of dementia, is caused by the degeneration of the central nervous system (CNS). A previous study reported that signal transducer and activator of transcription 3 (STAT3) is activated during AD development; nonetheless, the related mechanism remains unknown. Thus, this study used a cell model to explore whether and how the protein inhibitor of activated STAT3 (PIAS3) is involved in AD development. Methods Cerebrospinal fluid (CSF) specimens of 30 patients with AD and 10 normal participants were included in this study. SH-SY5Y cells were used to constructed AD model. Relevant indices were then detected and analyzed. Results The results showed that compared with the control group, PIAS3 expression was substantially decreased in patients with AD and amyloid beta (Aβ)-treated SH-SY5Y cells. PIAS3 overexpression was able to reverse the detrimental effects of Aβ treatment on cell survival and growth. Further, it could also ameliorate apoptosis and oxidative stress in Aβ-treated SH-SY5Y cells. Additionally, PIAS3 was shown to reduce the activated form of STAT3 and increase the activity of the downstream Nestin/nuclear factor erythroid 2-related factor/heme oxygenase-1 pathway. Conclusions STAT3 reactivation by colivelin treatment negated the influence of PIAS3 on the survival, growth, apoptosis, and oxidative stress of Aβ-treated SH-SY5Y cells.

Accelerated Aβ Generation in a Cell Model of Alzheimer's Disease-related Endosomal–Lysosomal System Upregulation

2003 ◽  
pp. 461-467
Author(s):  
Paul M. Mathews ◽  
Carolyn B. Guerra ◽  
Ying Jiang ◽  
Benjamin H. Kao ◽  
Ravi Dinakar ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cell Model ◽  
Model Of Alzheimer’S Disease ◽  
A Cell ◽  
Lysosomal System ◽  
Aβ Generation

scholarly journals Root-Securing and Brain-Fortifying Liquid Upregulates Caveolin-1 in Cell Model with Alzheimer’s Disease through Inhibiting Tau Phosphorylation

2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Depei Yuan ◽  
Chuhua Zeng ◽  
Qianfeng Chen ◽  
Fengjie Wang ◽  
Lin Yuan ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Tau Protein ◽  
Hippocampal Neurons ◽  
Cell Model ◽  
Tau Phosphorylation ◽  
Caveolin 1 ◽  
Sd Rats ◽  
A Cell ◽  
Underlying Mechanisms

In order to explore the effect of root-securing and brain-fortifying Liquid- (RSBFL-) mediated caveolin-1 (CAV-1) on phosphorylation of Tau protein and to uncover underlying mechanisms of RSBFL for the prevention and treatment of Alzheimer’s disease (AD), hippocampal neurons isolated from neonatal SD rats and cultured in DMEM-F12 medium were induced by exogenous Aβ1–42 to establish a cell model with AD. Meanwhile, pEGFP-C1-CAV1 and CAV1-shRNA plasmids were transfected into hippocampal neurons for CAV-1 overexpression and silence, respectively. The serum containing RSBFL was prepared for the intervention of AD model cells. The expression of CAV-1, GSK-3β, and p-Tau in normal hippocampal neurons and AD model cells in the presence of serum containing RSBFL was evaluated. The model hippocampal neurons with AD induced by Aβ1–42 revealed an obvious CAV-1 inhibition, enhanced GSK-3βactivity, and abnormal Tau phosphorylation. In contrast, the treatment with serum containing RSBFL could upregulate CAV-1 in AD hippocampal neurons (P<0.05) with improved p-GSK-3βSer9and reduced p-GSK-3βTyr216(P<0.01), as well as suppressed abnormal phosphorylation of Tau protein. Therefore, RSBFL has an excellent protective effect on hippocampal neurons through increasing CAV-1 expression, inhibiting GSK-3βactivity, and reducing excessive abnormal phosphorylation of Tau protein.

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