title: Apolipoprotein E epsilon4 allele differently affects the patterns of neuropsychological presentation in early- and late-onset Alzheimer's disease patients.
abstract: The presence of the apolipoprotein E (APOE) epsilon4 allele is a definite risk factor for the onset of Alzheimer's disease (AD). Its presence seems to affect especially the memory in the early stage of the disease, but the effect on the progression of the disease and survival is still controversial. Some longitudinal studies could be influenced by variables other than APOE, such as the response to medical treatment, rehabilitation therapy and inclusion of patients at different stages of progression at baseline. Moreover, the inclusion in the same study sample of patients of different ages at onset of the disease (below 65 or above 80 years) appears arbitrary. In our study, we evaluated a population of newly diagnosed untreated AD patients at their first neuropsychological examination and with the onset of their first symptoms not longer than 3 years ago. In order to analyse the different effects of the APOE epsilon4 allele on the different ages at the onset of the disease, we split the study sample into two groups: (1) subjects under 65 years [early-onset AD (EOAD); n = 30] and subjects over 70 years [late-onset AD (LOAD); n = 41], excluding subjects with an age of onset between 66 and 69 years. Our results show that the APOE epsilon4 allele carriers are characterised by a different neuropsychological pattern at the disease onset; however, only in the EOAD group is this effect significant: in EOAD, the epsilon4 allele carriers obtained worse performances in learning, long-term verbal memory and general intelligence tasks. On the contrary, in LOAD patients, the pattern of cognitive impairment at the onset is not dependent on the possession of an epsilon4 allele in the genotype. Such data could suggest a careful control of the study sample concerning age at the onset of the disease since APOE could play a different role in EOAD and LOAD mainly due to the different pathogenic mechanism at the onset and evolution of AD.
authors.affiliation: Department of Neurology, Catholic University of Rome, Rome, Italy. cmarra@rm.unicatt.it
authors.forename: Camillo
authors.initials: C
authors.lastname: Marra
authors.forename: Alessandra
authors.initials: A
authors.lastname: Bizzarro
authors.forename: Antonio
authors.initials: A
authors.lastname: Daniele
authors.forename: Lara
authors.initials: L
authors.lastname: De Luca
authors.forename: Monica
authors.initials: M
authors.lastname: Ferraccioli
authors.forename: Alessandro
authors.initials: A
authors.lastname: Valenza
authors.forename: Christina
authors.initials: C
authors.lastname: Brahe
authors.forename: Francesco Danilo
authors.initials: FD
authors.lastname: Tiziano
authors.forename: Guido
authors.initials: G
authors.lastname: Gainotti
authors.forename: Carlo
authors.initials: C
authors.lastname: Masullo
mesh_terms: D000367:Age Factors; D000368:Aged; D000369:Aged, 80 and over; D000483:Alleles; D000544:Alzheimer Disease / Q000175:diagnosis* / Q000235:genetics*; D053327:Apolipoprotein E4; D001057:Apolipoproteins E / Q000235:genetics*; D001284:Atrophy; D001921:Brain / Q000473:pathology; D018450:Disease Progression; D005260:Female; D005838:Genotype; D006801:Humans; D008297:Male; D008875:Middle Aged; D009483:Neuropsychological Tests / Q000706:statistics & numerical data*; D012307:Risk Factors; D012384:Rome
chemical_list: D053327:Apolipoprotein E4; D001057:Apolipoproteins E