Acetyl-L-carnitine-induced up-regulation of heat shock proteins protects cortical neurons against amyloid-beta peptide 1–42-mediated oxidative stress and neurotoxicity: Implications for Alzheimer's disease

2006 ◽  
Vol 84 (2) ◽  
pp. 398-408 ◽  
Author(s):  
Hafiz Mohmmad Abdul ◽  
Vittorio Calabrese ◽  
Menotti Calvani ◽  
D. Allan Butterfield
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Heat Shock ◽  
Heat Shock Proteins ◽  
Amyloid Beta ◽  
Cortical Neurons ◽  
Amyloid Beta Peptide ◽  
Beta Peptide ◽  
Shock Proteins

scholarly journals Oxidative stress and the amyloid beta peptide in Alzheimer’s disease

Redox Biology ◽  
2018 ◽  
Vol 14 ◽  
pp. 450-464 ◽  
Author(s):  
C. Cheignon ◽  
M. Tomas ◽  
D. Bonnefont-Rousselot ◽  
P. Faller ◽  
C. Hureau ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Beta ◽  
Amyloid Beta Peptide ◽  
Beta Peptide

scholarly journals Neuroprotective Effect of ent-Kaur-15-en-17-al-18-oic Acid on Amyloid Beta Peptide-Induced Oxidative Apoptosis in Alzheimer’s Disease

Molecules ◽  
2019 ◽  
Vol 25 (1) ◽  
pp. 142 ◽  
Author(s):  
Caiyun Zhang ◽  
Xingming Zhao ◽  
Shiqi Lin ◽  
Fangyuan Liu ◽  
Jiahui Ma ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Beta ◽  
Neuroprotective Effect ◽  
B Cell Lymphoma ◽  
Nuclear Factor Κb ◽  
Amyloid Beta Peptide ◽  
Nuclear Factor ◽  
Beta Peptide

ent-Kaur-15-en-17-al-18-oic acid, extracted from the Chinese well known folk herb Leontopodium longifolium, performed a significantly neuroprotective effect on amyloid beta peptide 25-35 (Aβ25-35)-induced SH-SY5Y cells neurotoxicity in Alzheimer’s disease. The results demonstrated that this compound maintained oxidative stress balance, reduced levels of reactive oxygen species (ROS), malondialdehyde (MDA), and improved contents of glutathione (GSH) and superoxide dismutase (SOD) without obvious cytotoxicity. This compound also obviously relieved oxidative stress-induced apoptosis associated with p53 and nuclear factor κB (NF-κB) pathways accompanied by upregulating B-cell lymphoma-2 (bcl-2) and downregulating p53, nuclear factor κB (NF-κB), Bax, Cleaved-caspase 3, and Cytochrome C protein expressions further. Briefly, ent-kaur-15-en-17-al-18-oic acid protected cells from oxidative apoptosis associated with p53 and NF-κB pathways.

Detecting bioactive amyloid beta peptide species in Alzheimer's disease

2004 ◽  
Vol 91 (3) ◽  
pp. 648-656 ◽  
Author(s):  
Yuanbin Liu ◽  
Richard Dargusch ◽  
Cindy Banh ◽  
Carol A. Miller ◽  
David Schubert
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Beta ◽  
Amyloid Beta Peptide ◽  
Beta Peptide

scholarly journals Quantitative phosphoproteomics of Alzheimer's disease reveals cross-talk between kinases and small heat shock proteins

PROTEOMICS ◽  
2014 ◽  
Vol 15 (2-3) ◽  
pp. 508-519 ◽  
Author(s):  
Eric B. Dammer ◽  
Andrew K. Lee ◽  
Duc M. Duong ◽  
Marla Gearing ◽  
James J. Lah ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Heat Shock ◽  
Heat Shock Proteins ◽  
Cross Talk ◽  
Small Heat Shock Proteins ◽  
Shock Proteins ◽  
Quantitative Phosphoproteomics

scholarly journals Heat Shock Proteins in Alzheimer’s Disease: Role and Targeting

2018 ◽  
Vol 19 (9) ◽  
pp. 2603 ◽  
Author(s):  
Claudia Campanella ◽  
Andrea Pace ◽  
Celeste Caruso Bavisotto ◽  
Paola Marzullo ◽  
Antonella Marino Gammazza ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Heat Shock ◽  
Heat Shock Proteins ◽  
Molecular Chaperones ◽  
Protein Misfolding ◽  
Point Of View ◽  
Toxic Species ◽  
Shock Proteins

Among diseases whose cure is still far from being discovered, Alzheimer’s disease (AD) has been recognized as a crucial medical and social problem. A major issue in AD research is represented by the complexity of involved biochemical pathways, including the nature of protein misfolding, which results in the production of toxic species. Considering the involvement of (mis)folding processes in AD aetiology, targeting molecular chaperones represents a promising therapeutic perspective. This review analyses the connection between AD and molecular chaperones, with particular attention toward the most important heat shock proteins (HSPs) as representative components of the human chaperome: Hsp60, Hsp70 and Hsp90. The role of these proteins in AD is highlighted from a biological point of view. Pharmacological targeting of such HSPs with inhibitors or regulators is also discussed.

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