A study from the Buck Institute for Age Research offers a revolutionary new model for Alzheimer’s disease. They have discovered a naturally occurring protein that provides a new therapeutic target, and suggests that Alzheimers is a disorder involving an imbalance in signaling between neurons. Read the complete report of research in Cell Death and Differentiation.
A novel intracellular signaling pathway mediated FE65 and APP
Tadashi Nakaya, Ph.D.
Head of Laboratory, Hokkaido University
Graduate School of Pharmaceutical Sciences
10:00 am – 11:00 am, Monday, September 15, 2008
15th Floor Conference room, WRB
Recommended Review Article:
McLoughlin, D.M.; & Miller, C.C.J. 2008. The FE65 proteins and Alzheimer’s disease. Journal of Neuroscience Research. 86(4):744-754. (please order copies from the Markus Library)
Nakaya, T.; Kawai, T.; & Suzuki, T. 2008. Regulation of FE65 Nuclear Translocation and Function by Amyloid β-Protein Precursor in Osmotically Stressed Cells. The Journal of Biological Chemistry. 283(27):19119-19131.
Müller, T.; et al. 2008. The amyloid precursor protein intracellular domain (AICD) as modulator of gene expression, apoptosis, and cytoskeletal dynamics—Relevance for Alzheimer’s disease. Progress in Neurology. 85(4):393-406.
Nakaya, T.; & Suzuki, T. 2006. Role of APP phosphorylation in FE65-dependent gene transactivation mediated by AICD. Genes to Cells. 11(6):633-645.