RESUMO
Alzheimer's disease (AD) is a severe neurodegenerative disorder characterized by cognitive decline. Prodromal stage of AD, also called mild cognitive impairment (MCI), especially its amnestic type (aMCI), precedes dementia stage of AD. There are currently no reliable diagnostic biomarkers of AD in the blood. Alzheimer's disease is accompanied by increased oxidative stress in brain, which leads to oxidative damage and accumulation of free radical reaction end-products. In our study, specific products of lipid peroxidation in the blood of AD patients were studied. Lipophilic extracts of erythrocytes (AD dementia = 19, aMCI = 27, controls = 16) and plasma (AD dementia = 11, aMCI = 17, controls = 16) were analysed by fluorescence spectroscopy. The level of these products is significantly increased in erythrocytes and plasma of AD dementia and aMCI patients versus controls. We concluded that oxidative stress end-products are promising new biomarkers of AD, but further detailed characterisation of these products is needed.
Assuntos
Doença de Alzheimer/sangue , Lipídeos/sangue , Idoso , Idoso de 80 Anos ou mais , Eritrócitos/metabolismo , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Espectrometria de FluorescênciaRESUMO
Apolipoprotein (APOE) É4 is a well-known risk factor for late-onset Alzheimer's disease (AD), but other AD-related gene polymorphisms might also be important, such as the polymorphism within the brain-derived neurotrophic factor (BDNF) gene. Carriage of BDNF Val66Met has been associated with faster cognitive decline and greater hippocampal atrophy in cognitively normal elderly. Thus, we examined the effects of the concurrent presence of APOE and BDNF polymorphisms on cognitive functions and brain morphometry in amnestic mild cognitive impairment (aMCI) patients. 107 aMCI patients (mean ageâ=â72.2) were recruited from the Czech Brain Aging Study and, based on APOE and BDNF genes polymorphisms, were divided into four groups: É4-BDNFVal/Val (nâ=â37), É4-BDNFMet (nâ=â19), É4+BDNFVal/Val (nâ=â35), and É4+BDNFMet (nâ=â16). All patients underwent clinical examination, magnetic resonance imaging, and complex neuropsychological battery. The combination of APOEÉ4+ and BDNF Met was associated with significantly worse memory performance in immediate and delayed recall compared to other polymorphism groups. We did not observe increased atrophy in areas related to memory function in the É4+BDNFMet group. Our findings suggest that carriage of É4+BDNFMet is associated with more pronounced memory dysfunction, a typical feature of early AD, but not with structural brain changes in aMCI patients. These findings suggest that in APOEÉ4/BDNF Met carriers, synaptic dysfunction affecting memory may precede pronounced structural changes.