Poster session : Memory defects in transgenic tau mice

Alzheimer's disease (AD), the most common cause of dementia afflicting 24 million people worldwide, has been identified as one of the major causes of disability and death by various health organizations. Neuropathological hallmarks include brain Beta-amyloid deposition and neurofibrillary tau-tangles, but progressive cognitive deterioration essentially characterizes this disorder at the behavioural level. Genetically modified mice are important research models for the study of pathogenic mechanisms of AD, and in the search for effective therapeutic strategies. Therefore, two transgenic mice strains expressing a human tau fragment, the 1st aggregating oK280 (PRO-aggregation of tau) and the 2nd a non-aggregating version (ANTI-aggregation of tau) of the same peptide were compared to nontrangenic littermates (CTRL or control animals) on a behavioral test battery. The battery included neuromotor tests (grip strength, rotarod, and cage activity), exploratory tests (open field and social exploration), and learning and memory tests (passive avoidance task and Morris water maze). Moreover neuroplasticity in the CA-1 region of hippocampal slices from the same mice was measured by long-term potentation (LTP) using a single theta-burst, and paired-pulse stimulation. Results show that the PRO mice were impaired in the single trial retention test (passive avoidance task), and more important in learning the Morris water maze compared to ANTI and CTRL mice. All 3 groups had normal sensorimotor function, highlighting the specificity of the memory deficit. Furthermore, the PRO mice showed a deficiency in hippocampal synaptic plasticity, as assessed by LTP and paired-pulse measures. These changes in neuroplasticity correlated with behavioural readouts of cognitive functionsstatus: publishe