Caspase Activation and Caspase-Mediated Cleavage of APP Is Associated with Amyloid β-Protein-Induced Synapse Loss in Alzheimer’s Disease

Author:

Park Goonho,Nhan Hoang S.,Tyan Sheue-Houy,Kawakatsu Yusuke,Zhang Carolyn,Navarro Mario,Koo Edward H.

Funder

NIH

NMRC

UCSD ADRC Pilot

BrightFocus ADR

NINDS

Publisher

Elsevier BV

Subject

General Biochemistry, Genetics and Molecular Biology

Reference78 articles.

1. C-terminal cleavage of the amyloid-beta protein precursor at Asp664: a switch associated with Alzheimer’s disease;Banwait;J. Alzheimers Dis.,2008

2. The intracellular threonine of amyloid precursor protein that is essential for docking of Pin1 is dispensable for developmental function;Barbagallo;PLoS ONE,2011

3. Neuronal activity regulates the regional vulnerability to amyloid-β deposition;Bero;Nat. Neurosci.,2011

4. The amyloid precursor protein intracellular domain-fe65 multiprotein complexes: a challenge to the amyloid hypothesis for Alzheimer’s disease?;Bórquez;Int. J. Alzheimers Dis.,2012

5. Importance of the caspase cleavage site in amyloid-β protein precursor;Bredesen;J. Alzheimers Dis.,2010

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