| Affiliation: | 1.INSERM U360, Recherches Epidémiologiques en Neurologie et Psychopathologie,H?pital de la Salpêtrière,Paris Cedex 13,France;2.INSERM E0361, Pathologies du système nerveux: recherche épidémiologique et clinique,H?pital La Colombière,Montpellier Cedex 5,France;3.INSERM U508,Institut Pasteur de Lille,Lille Cedex,France;4.Laboratoire de Neuropathologie R Escourolle, Association Claude Bernard,Université Pierre et Marie Curie, H?pital de la Salpêtrière,Paris Cedex 13,France;5.Service d'Anatomie Pathologique,H?pital de Hautepierre,Strasbourg Cedex,France |
| Abstract: | We studied whether codon 129 polymorphism of the PrP gene modulates the presence of tau- and Abeta-associated lesions among 188 patients over 70 years of age without evidence of dementia. Val allele carriers, either heterozygotes or homozygotes, were more frequently affected by Abeta-associated lesions than non Val allele carriers, whereas there were no differences for tau-positive neurones. Val allele carriers also had more focal and diffuse Abeta deposits. This association was most significant in the highest Braak's stages for neurofibrillary tangles (>/=III). In this group, cases with at least one Val allele had nearly twice as many Abeta-associated lesions. The most affected areas were the entorhinal cortex, TF-TH and the superior temporal cortex, where odds ratios for focal Abeta deposits ranged from 3.5 to 4.6. |
