Microtubule-associated protein tau in human fibroblasts with the Swedish Alzheimer mutation.

The principal neuropathological hallmarks of Alzheimer's disease (AD) are plaques containing amyloid beta peptide (Abeta) and tangles with hyperphosphorylated tau. Tau is predominantly found in the nervous system but has been reported in fibroblasts from individuals with and without AD. Abeta is also found outside the nervous system and is released three times more from cultured fibroblasts carrying the Swedish Alzheimer mutation in the amyloid precursor protein (APP) gene. In the present study, we determined tau levels in fibroblasts from carriers of the Swedish Alzheimer mutation and controls. We also characterized the expression of tau in these cells. Primary fibroblast cell lines from six individuals with and six without the mutation were investigated. ELISA measurements showed no statistically significant difference in tau levels between mutation-carrying cell lines and controls. On Western blot, four bands in the range of 47-67 kDa, corresponding to traditional tau isoforms, were detected with the Tau-l and AT 120 antibodies. Furthermore, four bands between 110-125 kDa were detected. We thus conclude that increased levels of Abeta do not seem to increase the levels of tau in human fibroblasts. We also suggest that several of the traditional tau isoforms as well as isoforms of higher molecular weights, big tau, are expressed in this cell type.