Sleep fragmentation significantly impacts cognitive function, as demonstrated by human studies linking it to an increased risk of Alzheimer’s Disease (AD), independent of age, sex, and education. Transgenic rodent models show a positive correlation between sleep fragmentation and Amyloid β (Aβ) plaque accumulation in the hippocampus and cortex. Additionally, some of these animal models exhibit sleep fragmentation prior to memory deficits and plaque deposition, which highlights the potential for sleep stability as a preventive measure against AD.
The goal of this project is to investigate the basic mechanisms by which the spike dynamics in midline thalamic circuits contribute to sleep stability and memory consolidation using optogenetics, pharmacology, and electrophysiology in behaving rats.
