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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 (<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M1\"><mml:mrow><mml:msup><mml:mrow><mml:mi>D<\/mml:mi><\/mml:mrow><mml:mrow><mml:mn fontstyle=\"italic\">2<\/mml:mn><\/mml:mrow><\/mml:msup><\/mml:mrow><\/mml:math>) was calculated between groups. To evaluate the diagnostic efficiency of this statistic<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M2\"><mml:mrow><mml:msup><mml:mrow><mml:mi>D<\/mml:mi><\/mml:mrow><mml:mrow><mml:mn fontstyle=\"italic\">2<\/mml:mn><\/mml:mrow><\/mml:msup><\/mml:mrow><\/mml:math>, the ROC models were used. The ROC curve was summarized by accuracy index and standard deviation. The<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M3\"><mml:mrow><mml:msup><mml:mrow><mml:mi>D<\/mml:mi><\/mml:mrow><mml:mrow><mml:mn fontstyle=\"italic\">2<\/mml:mn><\/mml:mrow><\/mml:msup><\/mml:mrow><\/mml:math>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.<\/jats:p>","DOI":"10.1155\/2014\/180741","type":"journal-article","created":{"date-parts":[[2014,1,9]],"date-time":"2014-01-09T10:22:55Z","timestamp":1389262975000},"page":"1-10","source":"Crossref","is-referenced-by-count":8,"title":["Spectral Analysis of EEG in Familial Alzheimer\u2019s Disease with E280A Presenilin-1 Mutation Gene"],"prefix":"10.1155","volume":"2014","author":[{"given":"Rene","family":"Rodriguez","sequence":"first","affiliation":[{"name":"Clinical Neurophysiology Department, Cuban Neuroscience Center, Havana, CP 10400, Cuba"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Francisco","family":"Lopera","sequence":"additional","affiliation":[{"name":"Antioquia University, Medellin, CP 1226, 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