Elevated vulnerability to oxidative stress-induced cell death and activation of caspase-3 by the Swedish amyloid precursor protein mutation

2001 ◽  
Vol 64 (2) ◽  
pp. 183-192 ◽  
Author(s):  
Anne Eckert ◽  
Barbara Steiner ◽  
Celio Marques ◽  
Steffen Leutz ◽  
Helmut Romig ◽  
...  
2008 ◽  
Vol 86 (11) ◽  
pp. 2476-2487 ◽  
Author(s):  
Kwang-Woo Ahn ◽  
Yuyoung Joo ◽  
Yoori Choi ◽  
Minji Kim ◽  
Sang Hyoung Lee ◽  
...  

2003 ◽  
Vol 278 (30) ◽  
pp. 28294-28302 ◽  
Author(s):  
Celio A. Marques ◽  
Uta Keil ◽  
Astrid Bonert ◽  
Barbara Steiner ◽  
Christian Haass ◽  
...  

1994 ◽  
Vol 168 (1-2) ◽  
pp. 254-256 ◽  
Author(s):  
Lars Lannfelt ◽  
Nenad Bogdanovic ◽  
Henrik Appelgren ◽  
Karin Axelman ◽  
Lena Lilius ◽  
...  

2000 ◽  
Vol 47 (2) ◽  
pp. 249-253 ◽  
Author(s):  
John B. J. Kwok ◽  
Qiao-Xin Li ◽  
Marianne Hallupp ◽  
Scott Whyte ◽  
David Ames ◽  
...  

Cells ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 3511
Author(s):  
Wafaa S. Ramadan ◽  
Saleh Alkarim

Patients suffering from Alzheimer’s disease (AD) are still increasing worldwide. The development of (AD) is related to oxidative stress and genetic factors. This study investigated the therapeutic effects of ellagic acid (EA) on the entorhinal cortex (ERC), which plays a major role in episodic memory, in the brains of an AD rat model. AD was induced using AlCl3 (50 mg/kg orally for 4 weeks). Rats were divided into four groups: control, AD model, EA (treated with 50 mg/kg EA orally for 4 weeks), and ADEA (AD rats treated with EA after AlCl3 was stopped) groups. All rats were investigated for episodic memory using the novel object recognition test (NORT), antioxidant serum biomarkers, lipid peroxidation, histopathology of the ERC, and quantitative PCR for the superoxide dismutase (SOD) gene. EA therapy in AD rats significantly increased the discrimination index for NORT and the levels of SOD, glutathione, and total antioxidant capacity. Lipid peroxidation products were decreased, and the neurofibrillary tangles and neuritic plaques in the ERC sections were reduced after EA administration. The decrease in ERC thickness in the AD group, caused by caspase-3-mediated apoptosis and neurotoxicity due to amyloid precursor protein, was modulated by the increased SOD mRNA expression. Adjustment of the ERC antioxidant environment and decreased oxidative stress under EA administration enhanced SOD expression, resulting in the modulation of amyloid precursor protein toxicity and caspase-3-mediated apoptosis, thereby restoring episodic memory.


Neurology ◽  
2003 ◽  
Vol 60 (6) ◽  
pp. 1020-1022 ◽  
Author(s):  
S. M. Greenberg ◽  
Y. Shin ◽  
T. J. Grabowski ◽  
G. E. Cooper ◽  
G. W. Rebeck ◽  
...  

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