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Altered expression of tau exon 10, clk2 and htra2-ß in post mortem brain of patients with Alzheimer’s disease
Pathological inclusions containing fibrillar aggregates of hyperphosphorylated tau protein are a characteristic feature in tauopathies, which include Alzheimer’s disease (AD). Tau transcripts undergo alternative splicing in the brain. Exon 10 codes for the second of four microtubule-binding repeats, and inclusion of exon 10 gives rise to isoforms containing four repeats (4R) whereas exclusion leads to isoforms containing only three (3R). A balanced level of these isoforms appears to be essential for neuronal function in the normal adult brain. Recent studies suggest that the SR-protein htra2-ß and the CDC-like kinase clk2 are involved in the regulation of alternative splicing of tau exon 10. In this study, we investigated the expression pattern of tau exon 10 and the levels of clk2 and htra2-ß isoforms in AD. Our preliminary results show an expression of tau, clk2 and htra2-ß isoforms in the frontal as well as in the temporal cortex in AD.