DEMONSTRATION OF A SPECIFIC PROFILE OF PA THOLOGICAL TAU-PROTEINS IN FRONTOTEMPORAL DEMENTIA CASES

We compared samples of different brain areas from patients with Alzhei mer's disease (AD), progressive supranuclear palsy (PSP), controls sub jects and from 4 patients who met the clinical and pathological criter ia for frontotemporal dementia (FTD), wing a Western blot analysis. We used polyclonal antibodies directed against Tau proteins and the mono clonal antibody AD2 for the immunodetection of the pathological Tau pr oteins which are the basic components of neurofibrillary degeneration. lit the PSP and AD cases, we respectively detected the abnormal Tau p roteins Gk and 69 and the Tau proteins 55, 64 and 69, systematically a ssociated with bands and smears, corresponding to catabolic products o r agregates of these abnormal Tau proteins. In FTD cases, the abnormal Tau proteins 55, 64 and 69 were also detected in the frontal and temp oral poles from the autopsied case and in the cortical biopsies. Howev er, the profiles were different because smears and proteolytics produc ts of Tau proteins were absent. There was no detection of abnormal Tau proteins in control brain homogenates and in biopsies from patients w ith other neurodegenerative disorders such as spongiform encephalopath ies or primitive gliosis. These results demonstrate that pathological Tau proteins are produced during FTD degenerating process, despite the absence of neurofibrillary lesions.