Home Institution: Fisk University
UCLA Mentor: Dr. Ketema Paul
Co-Author: Scott Vincent, Ketema Paul
Abstract:
Huntington’s Disease (HD) is an inherited disease caused by a repeated CAG DNA sequence with the Huntington (Htt) gene on the first exon. A polyglutamine repeat is produced when translation occurs leading to protein misfolding. In a mouse model of HD, BACHD mice showcase a disrupted circadian clock and disrupted sleep. While the BACHD mouse has prominent sleep phenotypes, such as abnormal NREM sleep timing and sleep fragmentation, the electrophysiological basis of these behaviors and any potential relationship to disease onset or progression have not yet been evaluated. Recent work in rats suggests that specific waveforms within NREM sleep might have distinct biological functions in sleep-dependent processes.
Using polysomnography, we evaluated NREM Slow Oscillations (SOs) and Delta Waves (DWs) of BACHD mice and their wild-type littermates under undisturbed and sleep deprived conditions. Raw EEG signal (400Hz) was collected and 10 second epochs were scored as NREM, REM, or wake. NREM SOs and DW were detected in 2-hour bins and normalized (Z-score) using a MATLAB script. We hypothesize that genotype-driven changes in NREM SOs or DWs may be responsible for the sleep disturbances seen in BACHD mice. We report an effect of genotype under baseline conditions which may support this hypothesis, but our current sample size is insufficient to generate statistical significance. Efforts to directly test our hypothesis are ongoing and the data is still being accumulated in the Paul Lab.
