scholarly journals Amyloid-.BETA. peptide metabolism and Alzheimer's disease

2003 ◽  
Vol 122 (1) ◽  
pp. 5-14 ◽  
Author(s):  
Nobuhisa IWATA ◽  
Takaomi C. SAIDO
2011 ◽  
Vol 2011 ◽  
pp. 1-13 ◽  
Author(s):  
Mallory Gough ◽  
Catherine Parr-Sturgess ◽  
Edward Parkin

Alzheimer's disease is a neurodegenerative condition characterized by an accumulation of toxic amyloid beta- (A-)peptides in the brain causing progressive neuronal death. A-peptides are produced by aspartyl proteinase-mediated cleavage of the larger amyloid precursor protein (APP). In contrast to this detrimental “amyloidogenic” form of proteolysis, a range of zinc metalloproteinases can process APP via an alternative “nonamyloidogenic” pathway in which the protein is cleaved within its A region thereby precluding the formation of intact A-peptides. In addition, other members of the zinc metalloproteinase family can degrade preformed A-peptides. As such, the zinc metalloproteinases, collectively, are key to downregulating A generation and enhancing its degradation. It is the role of zinc metalloproteinases in this “positive side of proteolysis in Alzheimer's disease” that is discussed in the current paper.


2004 ◽  
Vol 91 (3) ◽  
pp. 648-656 ◽  
Author(s):  
Yuanbin Liu ◽  
Richard Dargusch ◽  
Cindy Banh ◽  
Carol A. Miller ◽  
David Schubert

RSC Advances ◽  
2017 ◽  
Vol 7 (50) ◽  
pp. 31714-31724 ◽  
Author(s):  
Antonella Battisti ◽  
Antonio Palumbo Piccionello ◽  
Antonella Sgarbossa ◽  
Silvia Vilasi ◽  
Caterina Ricci ◽  
...  

This study suggests new concepts and potential difficulties in the design of novel drugs against diverse amyloidoses, including Alzheimer’s disease.


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