Plasma adiponectin array in women with Alzheimer's disease

Abstract

Introduction: Alzheimer's disease (AD) is a progressive and irreversible neurodegenerative disease. Typical features of AD include memory loss, social dysfunction, and physical impairment. Although the pathological findings in the central nervous system are well established, the aetiological factors are poorly known. Recent studies suggested the role of metabolic disturbances in the development of AD neurodegeneration. Adiponectin, an anti-inflammatory and metabolism regulating factor, was linked to AD. The aim was to examine whether adiponectin fractions combined with insulin/insulin resistance-associated metabolic parameters correlate with AD progression. Material and methods: The study comprised 98 women: 27 with moderate to severe AD, 31 with AD at early stage, and 40 healthy controls, matched for age and BMI. To evaluate memory impairment, the Mini-Mental State Examination (MMSE) was performed. Plasma total adiponectin and its high, medium, and low molecular weights were measured with ELISA. Anthropometric, clinical, and metabolic parameters were assessed. Correlations between adiponectin array and measured parameters were evaluated. Results: In comparison to the controls, enhanced levels of total and medium molecular weight adiponectin characterised AD individuals. In AD, we found correlations between adiponectin array, and anthropometric and biochemical parameters. After adjustment to BMI, a significant increase of the total adiponectin and high and medium molecular weight fractions was observed. A negative correlation between low molecular weight adiponectin and MMSE was found. Conclusions: Our results indicate a possible link between adiponectin variations and AD. We hypothesise that changes in adiponectin profile observed in AD result from compensatory mechanisms against neuropathological processes, as well as from adiponectin homeostasis impairment.