Imagine a world where sleep is like a peaceful river, flowing uninterrupted night after night. Well, in the case of Alzheimer’s disease (AD), that river gets tumultuous. Scientists have been studying the relationship between AD and sleep problems for some time now, and they’ve found that genetically modified mice can help unravel the mysteries. These little furry creatures, with boosted levels of amyloid beta or hyperphosphorylated tau, provide valuable insights into the progression of sleep disturbances in AD. By examining 15 different models of AD in mice, researchers have discovered changes in NREM and REM sleep duration, bout lengths, bout counts, and power spectra. They’ve also found common patterns of sleep deterioration across many models. Additionally, scientists are exploring how the accumulation of amyloid beta and tau tangles impacts sleep in AD. This review not only dives deep into the severity and timing of sleep problems in individual mouse models but also offers suggestions for future research and study design to enhance our understanding. So grab your virtual microscope and dive into the fascinating world of sleep disturbances in AD!
Alzheimer’s disease (AD) is the leading cause of dementia. The relationship between AD and sleep dysfunction has received increased attention over the past decade. The use of genetically engineered mouse models with enhanced production of amyloid beta (Aβ) or hyperphosphorylated tau has played a critical role in the understanding of the pathophysiology of AD. However, their revelations regarding the progression of sleep impairment in AD have been highly dependent on the mouse model used and the specific techniques employed to examine sleep. Here, we discuss the sleep disturbances and general pathology of 15 mouse models of AD. Sleep disturbances covered in this review include changes to NREM and REM sleep duration, bout lengths, bout counts and power spectra. Our aim is to describe in detail the severity and chronology of sleep disturbances within individual mouse models of AD, as well as reveal broader trends of sleep deterioration that are shared among most models. This review also explores a variety of potential mechanisms relating Aβ accumulation and tau neurofibrillary tangles to the progressive deterioration of sleep observed in AD. Lastly, this review offers perspective on how study design might impact our current understanding of sleep disturbances in AD and provides strategies for future research.
Dr. David Lowemann, M.Sc, Ph.D., is a co-founder of the Institute for the Future of Human Potential, where he leads the charge in pioneering Self-Enhancement Science for the Success of Society. With a keen interest in exploring the untapped potential of the human mind, Dr. Lowemann has dedicated his career to pushing the boundaries of human capabilities and understanding.
Armed with a Master of Science degree and a Ph.D. in his field, Dr. Lowemann has consistently been at the forefront of research and innovation, delving into ways to optimize human performance, cognition, and overall well-being. His work at the Institute revolves around a profound commitment to harnessing cutting-edge science and technology to help individuals lead more fulfilling and intelligent lives.
Dr. Lowemann’s influence extends to the educational platform BetterSmarter.me, where he shares his insights, findings, and personal development strategies with a broader audience. His ongoing mission is shaping the way we perceive and leverage the vast capacities of the human mind, offering invaluable contributions to society’s overall success and collective well-being.