Elevation of brain glucose and polyol-pathway intermediates with accompanying brain-copper deficiency in patients with Alzheimer’s disease: metabolic basis for dementia

• DOI: 10.1038/srep27524
• Publication Date: 2016-06-09T09:36:17Z
• Authors: Jingshu Xu; Paul Begley; Stephanie J. Church; Stefano Patassini; Selina McHarg; Nina Kureishy; Katherine A. Holl...; Henry J. Waldvogel; Hong Liu; Shaoping Zhang; Wanchang Lin; Karl Herholz; Clinton Turner; Beth J. Synek; Maurice A. Curtis; Jack Rivers-Auty; Catherine B. Lawr...; Katherine A. B. K...; Nigel M. Hooper; Emma R. L. C. Vardy; Donghai Wu; Richard D. Unwin; Richard L. M. Faull; Andrew W. Dowsey; Garth J. S. Cooper
• Keywords: Copper deficiency; Pathogenesis; Carbohydrate Metabolism

Abstract Impairment of brain-glucose uptake and brain-copper regulation occurs in Alzheimer’s disease (AD). Here we sought to further elucidate the processes that cause neurodegeneration AD by measuring levels metabolites metals brain regions undergo different degrees damage. We employed mass spectrometry (MS) measure seven post-mortem nine patients controls, plasma-glucose plasma-copper an ante-mortem case-control study. Glucose, sorbitol fructose were markedly elevated all regions, whereas copper was correspondingly deficient throughout (all P < 0.0001). In study, contrast, did not differ between controls. There pervasive defects glucose but no evidence for corresponding systemic abnormalities plasma. Elevation potentially contribute pathogenesis AD.