Brain Protein netrin-1 New Clue to Alzheimers

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.

Related Readings: Tadashi Nakaya


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)

Related Articles:

Nakaya, T.; Kawai, T.; & Suzuki, T.  2008.  Regulation of FE65 Nuclear Translocation and Function by Amyloid β-Protein Precursor in Osmotically Stressed CellsThe 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 diseaseProgress in Neurology.  85(4):393-406.

Nakaya, T.; & Suzuki, T.  2006.  Role of APP phosphorylation in FE65-dependent gene transactivation mediated by AICDGenes to Cells.  11(6):633-645.