ABSTRACT
Increased oxidative stress in the brain during the course of Alzheimer's disease (AD) leads to an imbalance of antioxidants and formation of free radical reaction end-products which may be detected in blood as fluorescent lipofuscin-like pigments (LFPs). The aim of this study was to evaluate and compare LFPs with plasma selenium concentrations representing an integral part of the antioxidant system. Plasma samples from subjects with AD dementia (ADD; n=11), mild cognitive impairment (MCI; n=17) and controls (n=12), were collected. The concentration of selenium was measured using atomic absorption spectroscopy. LFPs were analyzed by fluorescence spectroscopy and quantified for different fluorescent maxima and then correlated with plasma selenium. Lower levels of selenium were detected in MCI and ADD patients than in controls (P=0.003 and P=0.049, respectively). Additionally, higher fluorescence intensities of LFPs were observed in MCI patients than in controls in four fluorescence maxima and higher fluorescence intensities were also observed in MCI patients than in ADD patients in three fluorescence maxima, respectively. A negative correlation between selenium concentrations and LFPs fluorescence was observed in the three fluorescence maxima. This is the first study focused on correlation of plasma selenium with specific lipofuscin-like products of oxidative stress in plasma of patients with Alzheimer´s disease and mild cognitive impairment.
Subject(s)
Alzheimer Disease/blood , Brain/metabolism , Cognitive Dysfunction/blood , Lipid Peroxidation , Lipofuscin/blood , Oxidative Stress , Selenium/blood , Aged , Aged, 80 and over , Alzheimer Disease/diagnosis , Alzheimer Disease/physiopathology , Alzheimer Disease/psychology , Biomarkers/blood , Brain/physiopathology , Case-Control Studies , Cognitive Dysfunction/diagnosis , Cognitive Dysfunction/physiopathology , Cognitive Dysfunction/psychology , Female , Humans , Male , Mental Status and Dementia Tests , Middle Aged , Spectrometry, Fluorescence , Spectrophotometry, AtomicABSTRACT
Alzheimers disease is a severe neurodegenerative disorder and the most common cause of dementia in the population above 60 years of age. Beta-amyloid accumulation and neurofibrillary tangles formation in the brain precedes the development of Alzheimer's dementia by many years. As beta-amyloid accumulation inhibition failed as a treatment option, the theories on the Alzheimers disease pathophysio-lo-gy are being revised. In this context, research targets the role of inflammation as the possible trigger mechanism and accompanying process of neurodegeneration. This article summarizes some knowledge of the immune function of brain cells and its potential relation to Alzheimers disease progression in the light of the immune reaction hypothesis.
