Early cognitive dysfunction in the HD 51 CAG transgenic rat model of Huntington's disease.

摘要: Huntington’s disease (HD) is a neurodegenerative disorder in humans caused by an expansion of CAG trinucleotide repeat that produces choreic movements, which are preceded cognitive deficits. The HD transgenic rat (tgHD), contains the human mutation with 51 allele, exhibits motor deficits begin when these rats 12 months age. However, there no reports dysfunction occurring prior to this. To assess whether might precede tgHD rats, one group 9-month-old male homozygotic mutated genes and wild-type (WT) underwent three testing phases unique Spatial Operant Reversal Test (SORT) paradigm, as well assessment spontaneous activity. After testing, morphological histological examination brains were made. Results indicated acquired cued-response (Phase 1) portion SORT, but made significantly more errors during reversal 2) pseudorandomized reversals 3) study, compared WT rats. Analysis data using mathematical principles reinforcement revealed memory, motor, or motivational These results indicate early dysfunction, measured occur deficits, gross anatomical changes, cell loss repeats, suggest this protocol could provide useful screen for therapeutic studies.