Overexpression of amyloid precursor protein inhibits neurite outgrowth and disrupts cytoskeleton in N2a cells

• Published in: Chinese medical journal Vol. 117; no. 5; pp. 775 - 778
• Main Author: 王泽芬 王建枝
• Format: Journal Article
• Language: English
• Published: China Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China 01.05.2004
• Subjects: Amyloid beta-Protein Precursor - analysis; Amyloid beta-Protein Precursor - physiology; Animals; Cell Line, Tumor; Cytoskeleton - chemistry; Mice; N2a细胞; Neurites - physiology; Neuroblastoma - pathology; Neurofilament Proteins - analysis; Neurofilament Proteins - genetics; RNA, Messenger - analysis; 淀粉蛋白质; 神经丝; 神经突生长; 细胞骨架; 过表达; 阿尔海默氏病; β-amyloid precursor protein; neurite; neurofilament; Alzheimer's disease
• ISSN: 0366-6999; 2542-5641

There is considerable evidence suggesting that altered metabolism of β-amyloid precursor protein (APP) and accumulation of its β-amyloid (Aβ) fragment are key features of Alzheimer' s disease (AD). APP is a type Ⅰ integral membrane protein and consists of 695 - 770 amino acids encoded by differentially spliced mRNAs transcribed from a single gene located on human chromosome 21. The 695-amino acid APP is expressed preferentially in the brain. Aβ, the major component of senile plaques, is derived by proteolytic processing of APP by β-and γ-secretase and is constitutively released from most cells.