Park2-null/tau transgenic mice reveal a functional relationship between parkin and tau.

摘要: Mutations, haplotypes, and polymorphisms of tau Park-2 genes constitute risk factors for developing tauopathies. In order to analyze the possible relationship between parkin we generated a double-mutant mouse deficient expression overexpressing mutant protein (hTauVLW). Mice develop normally, although median survival rate is considerably reduced with respect wild type (45%). Aggregates phosphorylated in neurons reactive gliosis are quite abundant cortex hippocampus these mice. Moreover, while young transgenic mice hTauVLW immunostained transgene product observed both cell bodies dendrites, only detected neuronal when gene additionally deleted. DNA fragmentation was by TUNEL method, cerebral atrophy also present regions. The levels Hsp70 increased mice, CHIP lower Thus, combination deletion overexpression produces serious neuropathological effects, which reflect existence some proteins.