阿尔茨海默病与次黄嘌呤-鸟嘌呤磷酸核糖转移酶缺乏症（莱施-奈恩病）的嘌呤能失调存在基因表达异常。
Alzheimer's disease shares gene expression aberrations with purinergic dysregulation of HPRT deficiency (Lesch-Nyhan disease).
作者信息
Kang Tae Hyuk, Friedmann Theodore
机构信息
Department of Neurology, Yale University School of Medicine, 300 George Street, New Haven, CT 06511, USA.
Department of Pediatrics, University of California San Diego School of Medicine, 9500 Gilman Drive, La Jolla, CA 92093-0634, USA.
出版信息
Neurosci Lett. 2015 Mar 17;590:35-9. doi: 10.1016/j.neulet.2015.01.042. Epub 2015 Jan 27.
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.
对缺乏嘌呤生物合成功能次黄嘌呤鸟嘌呤磷酸核糖基转移酶（HPRT）并正在进行多巴胺能神经元分化的小鼠D3胚胎干细胞进行的转录组学研究表明，基因表达从神经元向神经胶质细胞发生了显著转变，并且多个基因的异常表达在阿尔茨海默病和其他中枢神经系统疾病中也有异常表现。这种基因失调可能表明多种中枢神经系统疾病中存在一些共同的致病代谢机制。
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