Serum zinc, copper, insulin and lipids in Alzheimer's disease epsilon 4 apolipoprotein E allele carriers

Citation
C. Gonzalez et al., Serum zinc, copper, insulin and lipids in Alzheimer's disease epsilon 4 apolipoprotein E allele carriers, EUR J CL IN, 29(7), 1999, pp. 637-642
Citations number
39
Categorie Soggetti
General & Internal Medicine","Medical Research General Topics
Journal title
EUROPEAN JOURNAL OF CLINICAL INVESTIGATION
ISSN journal
00142972 → ACNP
Volume
29
Issue
7
Year of publication
1999
Pages
637 - 642
Database
ISI
SICI code
0014-2972(199907)29:7<637:SZCIAL>2.0.ZU;2-K
Abstract
Background Copper (Cu) and zinc (Zn) have been implicated in the developmen t of Alzheimer's disease (AD) and, in this regard, Cu and Zn serum concentr ations have been analysed but with inconclusive results. Serum insulin, glu cose and cholesterol concentrations have been related to the apolipoprotein E genotype in non-AD populations. Design In this study, are have analysed the relationship between serum Cu, Zn, insulin, glucose and lipid parameters (cholesterol, triglycerides, apoA and apoB apolipoproteins) in AD and AD epsilon 4 apolipoprotein E carriers by multivariate analysis using logistic regression, including the variable s that showed a significance of P < 0.05 in the bivariate analysis. Results The results obtained show that epsilon 4 apoE allele is an independ ent AD risk factor (OR = 6.67, 95% CI = 2.59-17.16). In AD epsilon 4 apoE a llele carriers, we found significantly higher Zn, Cu and insulin serum conc entrations. Non-demented control subjects with at least one epsilon 4 apoE allele had the lowest serum insulin concentrations. There was no significan t association between epsilon 4 apolipoprotein E allele and lipid parameter s in the sample studied. Conclusions In AD we have found a significant association between higher se rum Zn, Cu and insulin concentrations and the presence of an epsilon 4 apoE allele, but only greater serum Zn concentration appears to be an independe nt risk factor associated with the development of AD.