Mitochondrial abnormalities in neuroectodermal cells stably expressing human amyloid precursor protein (hAPP751)

被引：38

作者：

Grant, SM

Shankar, SL

Chalmers-Redman, RME

Tatton, WG

Szyf, M

Cuello, AC

机构：

[1] McGill Univ, Dept Pharmacol & Therapeut, Montreal, PQ H3G 1Y6, Canada

[2] Mt Sinai Sch Med, Dept Neurol, New York, NY USA

来源：

NEUROREPORT | 1999年 / 10卷 / 01期

关键词：

amyloid precursor protein; electron microscopy; embryonal carcinoma; membrane potential; mitochondria;

D O I：

10.1097/00001756-199901180-00008

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

METABOLIC hypofunction is a common finding in a number of neurodegenerative diseases, including Alzheimer's disease (AD). The strong linkage between the amyloid precursor protein (APP) and AD led us to examine whether over-expression of this protein in CNS-type cells had an effect on mitochondria. We found abnormal morphology in mitochondria of the neuroectodermal progeny of P19 cells stably transfected with human APP(751) In addition, the mitochondria of APP-transfected clones had a decreased mitochondrial membrane potential. These changes were independent of A beta toxicity and distinct from complex I inhibition. Our results have important implications for the earliest events in the pathophysiology of AD and, by extrapolation, for intervention therapies. (C) 1999 Lippincott Williams & Wilkins.

引用

页码：41 / 46

页数：6

共 24 条

[1] Transfer of beta-amyloid precursor protein gene using adenovirus vector causes mitochondrial abnormalities in cultured normal human muscle [J].