第679回　千葉県がんセンター研究局集談会のお知らせ

演題： 軸索輸送障害とアルツハイマー病：カニクイザル脳組織からの知見
The impairment of axonal transport is a potential risk factor for Alzheimer's disease: Findings from cynomolgus monkey brains

演者： 木村 展之 博士
（独立行政法人 医薬基盤研究所 霊長類医科学研究センター・疾患制御研究室）
Nobuyuki Kimura, DVM, Ph.D.
Laboratory of Disease Control, Tsukuba Primate Research Center (TPRC),
National Institute of Biomedical Innovation (NIBIO)

日時： 平成21年9月9日（水曜日） 午後4時30分～午後6時

場所： 千葉県がんセンター 西１階TV会議室

要旨： Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by two pathological hallmarks, senile plaques (SPs) and neurofibrillary tangles (NFTs), and categorized into two types, familial AD (FAD) caused by mutations of certain causative genes, and sporadic AD (SAD) caused by aging. Nowadays, transgenic mice harboring FAD-related genetic mutations are widely used, and such mutations likely accelerate ß-amyloid protein (Aß), the major component of SP, assembly through enhanced Aß production from amyloid precursor protein (APP). However, currently, there is no evidence that Aß is overproduced in SAD brains, suggesting that the pathogenesis of SAD might be different from that of FAD. Furthermore, because more then 80% AD patients are categorized to SAD but not FAD, it is quite important to clarify the pathological mechanism of SAD.
In aged cynomolgus monkey brain, SPs are spontaneously observed in the neocortex and consistently at ages over 25. Moreover, the amino acid sequence of Aß is completely consistent with that of human beings. Thus, the cynomolgus monkey is considered to be a useful animal model to investigate age-dependent Aß pathology. Here, I summarize our findings from monkey brains, and discuss the impaired axonal transport as a potential risk factor for AD.