scholarly journals Inhibitory effect of Cu(II)on Zn(II)-induced aggregation of amyloid beta peptide

2001 ◽  
Vol 41 (supplement) ◽  
pp. S44
Author(s):  
K. Suzuki ◽  
T. Miura ◽  
H. Takeuchi
2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Rona Banerjee

Mononuclear complexes of Curcumin with Cu(II) and Zn(II) have been synthesized and, characterized and their effects on the fibrillization and aggregation of amyloid-beta (Aβ) peptide have been studied. FTIR spectroscopy and atomic force microscopy (AFM) observations demonstrate that the complexes can inhibit the transition from less structured oligomers toβ-sheet rich protofibrils which act as seeding factors for further fibrillization. The metal complexes also impart more improved inhibitory effects than Curcumin on peptide fibrillization.


2010 ◽  
Vol 114 (34) ◽  
pp. 11261-11271 ◽  
Author(s):  
Lian Hong ◽  
Tessa M. Carducci ◽  
William D. Bush ◽  
Christopher G. Dudzik ◽  
Glenn L. Millhauser ◽  
...  

Author(s):  
Saurav Chakraborty ◽  
Jyothsna ThimmaReddygari ◽  
Divakar Selvaraj

The Alzheimer disease is a age related neurodegenerative disease. The factors causing alzheimer disease are numerous. Research on humans and rodent models predicted various causative factors involved in Alzheimer disease progression. Among them, neuroinflammation, oxidative stress and apoptosis play a major role because of accumulation of extracellular amyloid beta peptides. Here, the clearance of amyloid beta peptide plays a major role because of the imbalance in the production and clearance of the amyloid beta peptide. Additionally, neuroinflammation by microglia, astrocytes, cytokines, chemokines and the complement system also have a major role in Alzheimer disease. The physiological clearance pathways involved in amyloid beta peptide are glymphatic, vascular and immune pathways. Amyloid precursor protein, low density lipoprotein receptor-related protein 1, receptor for advanced glycation end product, apolipoprotein E, clusterin, aquaporin 4, auto-antibodies, complement system, cytokines and microglia are involved in amyloid beta peptide clearance pathways across the blood brain barrier. The plaque formation in the brain by alternative splicing of amyloid precursor protein and production of misfolded protein results in amyloid beta agglomeration. This insoluble amyloid beta leads to neurodegenerative cascade and neuronal cell death occurs. Studies had shown disturbed sleep may be a risk factor for dementia and cognitive decline. In this review, the therapeutic targets for alzheimer disease via focussing on pathways for amyloid beta clearance are discussed.


2009 ◽  
Vol 999 (999) ◽  
pp. 1-6 ◽  
Author(s):  
L. Millucci ◽  
L. Ghezzi ◽  
G. Bernardini ◽  
A. Santucci

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