Transgenic expression of the FTDP-17 tauV337M mutation in brain dissociates components of executive function in mice

摘要: Frontotemporal lobe dementia (FTD) is a heterogeneous range of disorders, subset which arise from fully penetrant, autosomal dominant point mutations in the gene coding for microtubule associated protein tau. These genetic tauopathies are with complex behavioural/cognitive disturbances, including compromised executive function. In present study, we modelled effects FTD Parkinsonism linked to chromosome 17 (FTDP-17) tauV337M mutation (known as Seattle Family A mutation) expressed mice on processes using novel murine analogue Stroop task. Employing biconditional discrimination procedures, Experiment 1 showed that normal mice, but not excitotoxic lesions medial prefrontal cortex, were able use context cues resolve response conflict generated by incongruent stimulus compounds. contrast predictions, resolution was disrupted (Experiment 2). However, while appropriate actions goal-directed wild-type performance 3). The results indicate disrupts, selectively, related