β-Amyloid-Associated Free Radical Oxidative Stress and Neurotoxicity:  Implications for Alzheimer's Disease

1997 ◽  
Vol 10 (5) ◽  
pp. 495-506 ◽  
Author(s):  
D. Allan Butterfield
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Free Radical ◽  
Β Amyloid

scholarly journals Pharmacological inhibition of G9a/GLP restores cognition and reduces oxidative stress, neuroinflammation and β-Amyloid plaques in an early-onset Alzheimer’s disease mouse model

Aging ◽  
2019 ◽  
Vol 11 (23) ◽  
pp. 11591-11608 ◽  
Author(s):  
Christian Griñán-Ferré ◽  
Laura Marsal-García ◽  
Aina Bellver-Sanchis ◽  
Shukkoor Muhammed Kondengaden ◽  
Ravi Chakra Turga ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Early Onset ◽  
Amyloid Plaques ◽  
Pharmacological Inhibition ◽  
Early Onset Alzheimer’S Disease ◽  
Β Amyloid

scholarly journals Ingredients in Zijuan Pu’er Tea Extract Alleviate β-Amyloid Peptide Toxicity in a Caenorhabditis elegans Model of Alzheimer’s Disease Likely through DAF-16

Molecules ◽  
2019 ◽  
Vol 24 (4) ◽  
pp. 729 ◽  
Author(s):  
Fangzhou Du ◽  
Lin Zhou ◽  
Yan Jiao ◽  
Shuju Bai ◽  
Lu Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Caenorhabditis Elegans ◽  
Protective Effect ◽  
Nuclear Translocation ◽  
Amyloid Β ◽  
Amyloid Peptide ◽  
C Elegans ◽  
Β Amyloid

Amyloid-β, one of the hallmarks of Alzheimer’s disease (AD), is toxic to neurons and can also cause brain cell death. Oxidative stress is known to play an important role in AD, and there is strong evidence that oxidative stress is associated with amyloid-β. In the present study we report the protective effect of Zijuan Pu’er tea water extract (ZTWE) and the mixture of main ingredients (+)-catechins, caffeine and procyanidin (MCCP) in ZTWE on β-amyloid-induced toxicity in transgenic Caenorhabditis elegans (C. elegans) CL4176 expressing the human Aβ1–42 gene. ZTWE, (+)-catechins, caffeine, procyanidin and MCCP delayed the β-amyloid-induced paralysis to different degrees. The MCCP treatment did not affect the transcript abundance of amyloid-β transgene (amy-1); however, Thioflavin T staining showed a significant decrease in Aβ accumulation compared to untreated worms. Further research using transgenic worms found that MCCP promoted the translocation of DAF-16 from cytoplasm to nucleus and increased the expression of superoxide dismutase 3 (SOD-3). In addition, MCCP decreased the reactive oxygen species (ROS) content and increased the SOD activity in CL4176 worms. In conclusion, the results suggested that MCCP had a significant protective effect on β-amyloid-induced toxicity in C. elegans by reducing β-amyloid aggregation and inducing DAF-16 nuclear translocation that could activate the downstream signal pathway and enhance resistance to oxidative stress.

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