RESUMO
Dementia is one of the most pressing public health problems with social and economic implication. The form called cognitive impairment non-dementia (CIND)represents a subclinical phase of dementia. Different studies have shown a possible effect of micro- and macro-nutrients on cognitive function. Trace elements, being involved in metabolic processes and redox reactions in the central nervous system (CNS), could influence the cognitive functions. This study evaluated the presence of an eventual correlation between serum trace element concentrations and cognitive function in a group of subjects with CIND and manifest dementia (Alzheimer dementia = AD, and vascular dementia = VaD), and compared them with a control group. Thirty -five patients were enrolled in this study. Each patient underwent a clinical and biochemical examination. We also performed a neuropsychological and functional assessment (the Milan overall dementia assessment = MODA, activities of daily living = ADL, and instrumental activities of daily living = IADL), and a computerized tomographic (CT) cerebral scan. Patients were than divided in 4 groups according to the obtained diagnosis (Controls, CIND, AD, VaD). The presence of any acute or chronic conditions, affecting cognitive functions, was considered as exclusion criteria. A blood sample was collected to determine iron (Fe), zinc (Zn), manganese (Mn), selenium (Se), cobalt (Co), chromium (Cr), copper (Cu),molybdenum (Mo) and aluminium (Al) serum concentrations (chromatographic,spectrophotometric methods). In our cohort we found a positive correlation between cognitive function, expressed as the MODA score, and Se, Cr, Co and Fe serum levels,while a negative correlation was observed between MODA score, Cu and Al serum levels.Moreover, some statistically significant differences in Se, Cr, Co, Cu and Al concentrations were found among the groups. According to these results, we may suppose that Se, Cr and Co protect cognitive function, Cu influences the evolution of cognitive impairment, while Al contributes to the pathogenesis of AD.
