Affiliations: [a]
Laboratory of Molecular Biology, VA New Jersey Health Care System, Research & Development, East Orange, NJ, USA
| [b]
Laboratory of Molecular Biology, Bay Pines VA Healthcare System, Research and Development, Bay Pines, FL, USA
| [c]
Department of Pharmacology, Physiology, & Neuroscience ,Rutgers-New Jersey Medical School, Newark, NJ, USA
Correspondence:
[*]
Correspondence to: Bruce A. Citron, PhD, VA New Jersey Health Care System, Laboratory of Molecular Biology, Research and Development, Building 16, Room 16-176, 385 Tremont Ave., East Orange, NJ 07018, USA. Tel.: +1 973 676 1000 /Ex1-3686; E-mail: [email protected].
Abstract: An estimated 5 million Americans are living with Alzheimer's disease (AD), and there is also a significant impact on caregivers, with an additional 16 million Americans providing unpaid care for individuals with AD and other dementias. These numbers are projected to increase in the coming years. While AD is still without a cure, continued research efforts have led to better understanding of pathology and potential risk factors that could be exploited to slow disease progression. A bidirectional relationship between sleep deprivation and AD has been suggested and is well supported by both human and animal studies. Even brief episodes of inadequate sleep have been shown to cause an increase in amyloidβ and tau proteins, both well-established contributors toAD pathology. Sleep deprivation is also the most common consequence of post-traumatic stress disorder (PTSD). Patients with PTSD frequently present with sleep disturbances and also develop dementia at twice the rate of the general population accounting for a disproportionate representation of AD among U.S. Veterans. The goal of this review is to highlight the relationship triad between sleep deprivation, AD, and PTSD as well as their impact on molecular mechanisms driving AD pathology.
Keywords: Alzheimer’s disease, amyloid-β, post-traumatic stress disorder, sleep deprivation, tau
