Alzheimer's disease shares gene expression aberrations with purinergic dysregulation of HPRT deficiency (Lesch-Nyhan disease)

被引：16

作者：

Kang, Tae Hyuk ^{[1
]}

Friedmann, Theodore ^{[2
]}

机构：

[1] Yale Univ, Sch Med, Dept Neurol, New Haven, CT 06511 USA

[2] Univ Calif San Diego, Sch Med, Dept Pediat, La Jolla, CA 92093 USA

来源：

NEUROSCIENCE LETTERS | 2015年 / 590卷

基金：

美国国家卫生研究院;

关键词：

Neurogenesis; Neurodevelopment disease; Neurodegenerative disease; Alzheimer's disease; HPRT; Lesch-Nyhan disease; NEURONAL DIFFERENTIATION; RECEPTORS; GROWTH; NUCLEOTIDE; PATHWAYS; ACTIVATION; COMPLEX; PROTEIN; MODEL;

D O I：

10.1016/j.neulet.2015.01.042

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Transcriptomic studies of murine D3 embryonic stem (ES) cells deficient in the purinergic biosynthetic function hypoxanthine guanine phosphoribosyltransferase (HPRT) and undergoing dopaminergic neuronal differentiation has demonstrated a marked shift from neuronal to glial gene expression and aberrant expression of multiple genes also known to be aberrantly expressed in Alzheimer's and other CNS disorders. Such genetic dysregulations may indicate some shared pathogenic metabolic mechanisms in diverse CNS diseases. (C) 2015 Elsevier Ireland Ltd. All rights reserved.

引用

页码：35 / 39

页数：5

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