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Neurosci Lett. 2015 Mar 17;590:35-9. doi: 10.1016/j.neulet.2015.01.042. Epub 2015 Jan 27.

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

Author information

1
Department of Neurology, Yale University School of Medicine, 300 George Street, New Haven, CT 06511, USA.
2
Department of Pediatrics, University of California San Diego School of Medicine, 9500 Gilman Drive, La Jolla, CA 92093-0634, USA. Electronic address: tfriedmann@ucsd.edu.

Abstract

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.

KEYWORDS:

Alzheimer’s disease; HPRT; Lesch–Nyhan disease; Neurodegenerative disease; Neurodevelopment disease; Neurogenesis

PMID:
25636690
DOI:
10.1016/j.neulet.2015.01.042
[Indexed for MEDLINE]
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