Abstract
Dysfunctions of vesicular transport are linked to neurodegenerative disease, including Alzheimer disease (AD). Amyloid β-prrotein precursor (APP) has been implicated in the development and progression of AD. Recent reports suggest that APP functions as cargo receptor for kinesin I. APP interacts with kinesin light chain (KLC) indirectly via JNK-interacting protein 1b (JIP1b). We have reported that APP associates with Alcadein, a novel type I membrane protein, in neuron through their cytoplasmic interaction with X11-like (X11L) protein. We also found that Alcadein associates with KLC directly, thus Alcadein and APP/JIP1b competed for KLC. Alteration in APP- and Alcadein-transport system in neuron impairs the vesicle trafficking in axon, suggesting that inappropriate assignment of these cargos leads to neuronal malfunction and the degeneration in future. [J Physiol Sci. 2006;56 Suppl:S34]
