Capillary cerebral amyloid angiopathy identifies a distinct APOE ε4-associated subtype of sporadic Alzheimer’s disease
Primary neuronal cultures were treated with glutamate to induce an increase of Tau immunoreactivity similar to that observed in Alzheimer's disease. The Tau profile of neurones in culture before and after exposure to glutamate was analyzed on immunoblots with anti-Tau, anti-paired helical filaments (PHF) and antibody specific for modified Tau. Differences were observed between treated and control cultures: glutamate induced a shift of immunodetection from the lowest to the highest molecular weight Tau isoform and an acidification of Tau proteins. However, these modifications are not exactly those observed in Alzheimer's disease since we were not able to detect 'Alzheimer-type' epitopes on Tau proteins after the glutamate exposure.