Alzheimer;s disease (AD) is a multifactorial disease but its aetiology and pathophisiology are still not fully understood. Epidemiologic studies examining the association between lipids and dementia have reported conflicting results. High total cholesterol has been associated with both an increased, and decreased, risk of AD and/or vascular dementia (VAD), whereas other studies found no association. The aim of this study was to investigate the serum lipids concentration in patients with probable AD, as well as possible correlation between serum lipids concentrations and cognitive impairment. Our cross-sectional study included 30 patients with probable AD and 30 age and sex matched control subjects. The probable AD was clinically diagnosed by NINCDS-ADRDA criteria. Serum total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C) and triglyceride (TG) levels were determined at the initial assessment using standard enzymatic colorimetric techniques. Low-density lipoprotein cholesterol (LDL-C) and very low density lipoprotein cholesterol (VLDL-C) levels were calculated. Subjects with probable AD had significantly lower serum TG (p<0,01), TC (p<0,05), LDL-C (p<0,05) and VLDL-C (p<0,01) compared to the control group. We did not observe significant difference in HDL-C level between patients with probable AD and control subjects. Negative, although not significant correlation between TG, TC and VLDL-C and MMSE in patients with AD was observed. In the control group of subjects there was a negative correlation between TC and MMSE but it was not statistically significant (r = -0,28). Further studies are required to explore the possibility for serum lipids to serve as diagnostic and therapeutic markers of AD.

The evolution of homocysteine (Hcy) changes after acute myocardial infarction is still not elucidated. Serum Hcy concentration has been shown to increase between acute and convalescent period after myocardial infarction and stroke. Also a decrease in serum Hcy during acute phase was observed. It is still not clear whether the Hcy is a culprit or an innocent bystander in cardiovascular diseases. Addressing the discrepancies in Hcy changes in patients with acute myocardial infarction might give insight in Hcy role in cardiovascular diseases and offer implications both for the clinical interpretation and patients risk stratification. The aim of the study was to evaluate serum Hcy concentration changes during early post myocardial infarction. The study included 55 patients with AMI from the Clinics for Heart Diseases and Rheumatism at University of Sarajevo Clinics Centre. For Hcy analysis blood was collected on day 2 and 5 after the AMI onset. Serum Hcy concentration was determined quantitatively with fluorescent polarisation immunoassay on AxSYM system. Cluster analysis revealed two groups of AMI patients with different trends of serum Hcy changes. Increase in serum Hcy concentration was observed in 33 (60,0%) patients (AMI 1 group), while in 22 (40,0%) patients a decrease was observed (AMI 2 group). On day 2, patients in AMI 2 group had significantly higher mean Hcy concentration compared to AMI 1 group of patients (15,27+/-0,96 and 11,59+/-0,61 micromol/L p<0,05). On day 5, no significant difference in mean Hcy level between AMI 1 and AMI 2 group of patients was observed (14,86+/-1,1 vs. 12,75+/-0,74 micromol/L respectively). Significant differences between AMI 1 and AMI 2 patients were observed in VLDLC levels and CK-MB activity on day 2. Patients in AMI 1 group had significant increase in platelets count from day 2 to day 5 (230,1+/-11,6 vs. 244,2+/-11,0; p<0,05). Our study of serial Hcy changes in patients with AMI revealed two different patterns of Hcy changes in early post infarction period which might reflect two distinct populations of AMI patients. Although further research is necessary, possible explanation for the observed findings could be a different genetic background, vitamin and oxidative status of patients with AMI.