Researchers have discovered that brain inflammation may link Alzheimer’s disease risk with sleep disturbance, potentially aiding early detection and prevention efforts by identifying novel treatment targets at preclinical stages.
The study, published online today in the journal Sleep, examined whether inflammation affected specific brain waves called fast sleep spindles, which have been shown to promote long-term memory retention. Bryce Mander, Ph.D., UCI assistant professor of psychiatry and human behaviour and the study’s lead and co-corresponding author, said, “Our findings indicate that age-related increases in brain inflammation have a downstream effect on Alzheimer’s disease-related tau proteins and neuronal synaptic integrity. This results in deficits in the brain’s capacity to generate fast sleep spindles, which contribute to age-related memory impairment in older adults. Discovering these mechanisms is important in identifying at-risk individuals as early as possible and developing targeted interventions.”
Chronic activation of the brain's immune cells, called "glial cells," increases with age, elevating the production of beta-amyloid and tau proteins, the hallmarks of Alzheimer's disease.
Sleep disturbance has been linked to Alzheimer's disease pathology in the brain, and studies have indicated an association between sleep disturbance and inflammation. Selectively disrupted fast sleep spindles have been identified in normal aging and preclinical stages of Alzheimer's disease. Still, it has not been clear what causes this and what it means for memory impairment in older at-risk adults.
"We don't yet know whether anyone in this study will develop Alzheimer's disease dementia, but one of the reasons that our studies enroll participants in midlife is so that we can potentially detect problems before people develop disease symptoms," said co-author Barbara Bendlin, Ph.D., professor of medicine at the University of Wisconsin-Madison.
"These findings show that the effects of brain inflammation on sleep spindles and memory occur through its effects on neuronal activity and Alzheimer's disease-related proteins and are apparent even before pathological positivity," said Dr. Ruth Benca, the study's senior and co-corresponding author and Wake Forest professor and chair of psychiatry and behavioural medicine.
