Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.1.8 (cholinesterase)
 12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although serum cholinesterase (CHE) is elevated in some hyperlipidaemic subjects, the relationship between serum CHE and lipids in normolipidaemic subjects is scanty. Furthermore, serum CHE is reduced in conditions in which there is an acute phase response. Serum CHE activity was measured in 46 normal individuals (22 males and 24 females). There was no significant difference between the activity of serum CHE in males or females being 6.2 +/- 1.8 U1(-1) vs. 6.4 +/- 1.5 U1(-1) respectively (mean +/- SD). There was, however, a significant correlation between serum CHE and subject age (Spearman rho 0.35, p < 0.05). There was also a significant correlation between serum CHE and serum nonfasting triglyceride concentration (rho 0.34, p < 0.05) and also apolipoprotein B (rho 0.38, p < 0.05) but not serum cholesterol or HDL-cholesterol. Five serum acute phase proteins were measured namely serum alpha-1 antichymotrypsin (ACT), alpha-1-acid-glycoprotein (AGP), alpha-2-macroglobulin (AMG), C-reactive protein (CRP), haptoglobin (HAP). Only serum AGP showed a significant negative correlation with serum CHE (rho - 0.43, p < 0.02).
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PMID:Serum lipids, acute phase proteins and serum cholinesterase in normal subjects. 753 45

There is considerable enthusiasm for the prospect of using common polymorphisms (primarily single nucleotide polymorphisms; SNPs) in candidate genes to unravel the genetics of complex disease. This approach has generated a number of findings of loci which are significantly associated with sporadic Alzheimer's disease (AD). In the present study, a total of 15 genes of interest were chosen from among the previously published reports of significant association in AD. Genotyping was performed on polymorphisms within those genes (14 SNPs and one deletion) using Dynamic Allele Specific Hybridization (DASH) in 204 Swedish patients with sporadic late-onset AD and 186 Swedish control subjects. The genes chosen for analysis were; low-density lipoprotein receptor-related protein (LRP1), angiotensin converting enzyme (DCP1), alpha-2-macroglobulin (A2M), bleomycin hydrolase (BLMH), dihydrolipoyl S-succinyltransferase (DLST), tumour necrosis factor receptor superfamily member 6 (TNFRSF6), nitric oxide synthase (NOS3), presenilin 1 (PSEN1), presenilin 2 (PSEN2), butyrylcholinesterase (BCHE), Fe65 (APBB1), oestrogen receptor alpha (ESR1), cathepsin D (CTSD), methylenetetrahydrofolate reductase (MTHFR), and interleukin 1A (IL1A). We found no strong evidence of association for any of these loci with AD in this population. While the possibility exists that the genes analysed are involved in AD (ie they have weak effects and/or are population specific), results reinforce the need for extensive replication studies if we are to be successful in defining true risk factors in complex diseases.
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PMID:Lack of replication of association findings in complex disease: an analysis of 15 polymorphisms in prior candidate genes for sporadic Alzheimer's disease. 1143 25