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Journal of Biochemistry 2006 139(6):949-955; doi:10.1093/jb/mvj121
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© 2006 The Japanese Biochemical Society.

JB Minireview--Membrane Traffic in Physiology and Pathology

Trafficking of Alzheimer's Disease–Related Membrane Proteins and Its Participation in Disease Pathogenesis

Toshiharu Suzuki*, Yoichi Araki, Tohru Yamamoto and Tadashi Nakaya

Graduate School of Pharmaceutical Sciences, Hokkaido University, Kita 12–Nishi 6, Kita-ku, Sapporo 060-0812

* To whom correspondence should be addressed. Tel: +81-11-706-3250, Fax: +81-11-706-4991, E-mail: tsuzuki{at}pharm.hokudai.ac.jp

Alzheimer's disease (AD) is a common neurodegenerative disorder that causes senile dementia. The pathological characteristics are the appearance of neurofibrillary tangles comprising abnormally phosphorylated tau and senile plaques composed of amyloid ß-protein depositions. Amyloid ß-protein precursor (APP) and presenilin (PS) are known to be causative genes of familial AD. Recent analyses have documented that APP functions in the axonal transport of vesicles and PS regulates intracellular protein trafficking. Dystrophic neurites, in which APP and Alcadein accumulate in swollen axons, are also observed in AD brain. These pathological characteristics and the features of AD-related proteins suggest that AD is a disease of the vesicular transport system. Here we review recent progress of research on AD pathogenesis from the viewpoint of membrane trafficking.


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