%0 Journal Article
%T Spectral Analysis of EEG in Familial Alzheimer¡¯s Disease with E280A Presenilin-1 Mutation Gene
%A Rene Rodriguez
%A Francisco Lopera
%A Alfredo Alvarez
%A Yuriem Fernandez
%A Lidice Galan
%A Yakeel Quiroz
%A Maria Antonieta Bobes
%J International Journal of Alzheimer's Disease
%D 2014
%I Hindawi Publishing Corporation
%R 10.1155/2014/180741
%X To evaluate the hypothesis that quantitative EEG (qEEG) analysis is susceptible to detect early functional changes in familial Alzheimer's disease (AD) preclinical stages. Three groups of subjects were selected from five extended families with hereditary AD: a Probable AD group (18 subjects), an asymptomatic carrier (ACr) group (21 subjects), with the mutation but without any clinical symptoms of dementia, and a normal group of 18 healthy subjects. In order to reveal significant differences in the spectral parameter, the Mahalanobis distance ( ) was calculated between groups. To evaluate the diagnostic efficiency of this statistic , the ROC models were used. The ROC curve was summarized by accuracy index and standard deviation. The using the parameters of the energy in the fast frequency bands shows accurate discrimination between normal and ACr groups (area ROC = 0.89) and between AD probable and ACr groups (area ROC = 0.91). This is more significant in temporal regions. Theses parameters could be affected before the onset of the disease, even when cognitive disturbance is not clinically evident. Spectral EEG parameter could be firstly used to evaluate subjects with E280A Presenilin-1 mutation without impairment in cognitive function. 1. Introduction Alzheimer¡¯s disease (AD) is a neurodegenerative disorder in the elderly characterized by progressive dementia [1, 2]. The disorder probably begins many years before the first clinical symptoms are evident [3, 4]. Recent studies have demonstrated that during the presymptomatic phase, neuronal degeneration occurs even without the presence of clinical symptoms [5]. These make preclinical discrimination between people who will and will not ultimately develop AD critical for early treatment of the disease [6]. Neuropathological hallmarks of AD include macroscopic change as reduced brain weight with cortical atrophy and ventricular enlargements primarily due to neuronal loss in the temporal and parietal structures [7]. At the microscopic level, it can be found neurofibrillary tangles (intracellular aggregations of tau protein filaments) and amyloid plaques (extracellular aggregates of amyloid beta-peptides) that are particularly concentrated in the hippocampus, entorhinal cortex, and postcentral parietal neocortex. [2, 8, 9]. Recent advances in molecular genetics have allowed identifying individuals carrying defective genes predisposed to develop AD [10]. When the disease penetrance is high, the examination of apparently asymptomatic subjects carriers of defective genes allows early evaluation of different
%U http://www.hindawi.com/journals/ijad/2014/180741/