Early deficits in declarative and procedural memory dependent behavioral function in a transgenic rat model of Huntington's disease

摘要: In Huntington's disease (HD) cognitive deficits co-exist with motor impairments, both contributing to the overall symptomology. Despite short-term and working memory learning other non-motoric behavioral arising from damage frontostriatal loop being common in HD patients, most of experimental work transgenic animals focuses on symptoms. The rat model (tgHD) recapitulates many hallmark HD-like symptoms, such as huntingtin aggregates, cellular loss dysfunction, motor, some deficits. current study we tested tgHD rats two different cognitive, water maze competition paradigms learn more about impact transgene processing using hippocampal- striatal-based systems. had early robust function paradigms. Specifically, were impaired task acquisition committed procedural errors strongest phenotype amongst homozygote tgHD. Although capable declarative memory, their response patterns distinct wild-type animals. Wide spread aggregates observed at 13 months, but neither PET nor autoradiography indicated neuronal or dysfunction striatal dopamine receptor population. summary, showed a impairment prior any clear deficits, dysfunction. However, data not conclusive regarding how systems compromised precise nature underlying mechanism deficit requires further investigation.