AD Learning And Memory Loss Problems Mimic Jet Lag
Findings from a recent study published in the Journal of Alzheimer’s Disease revealed that chemical alterations in brain cells triggered by disruptions in the body’s day-night cycle may be an underlying cause of the memory and learning loss observed in Alzheimer’s disease (AD). The study, conducted by University of California researchers, is the first providing evidence that circadian rhythm-altering sleep disturbances identical to jet lag cause alterations in the brain and memory dysfunctions.
Patients suffering with AD often have sleep problems or experience alterations in their slumber schedule; however, the cause underlying these disruptions remains poorly understood. These novel findings could lead clinicians to put greater emphasis on the management of sleep patterns in people with mild cognitive impairment as well as in those at risk for AD. “The issue is whether poor sleep accelerates the development of Alzheimer’s disease or vice versa,” study author Gregory Brewer, who’s affiliated with UCI’s Institute for Memory Impairments and Neurological Disorders, said in a news release. “It’s a chicken-or-egg dilemma, but our research points to disruption of sleep as the accelerator of memory loss.”
To evaluate the association between memory and learning and circadian disturbances, researchers altered natural light-dark patterns with an eight-hour shortening of the dark period every three days in normal mice and in mouse models of AD. The resultant jet lag significantly reduced activity in both mice groups, with the team also observing that in water maze tests AD mice had significant impairments in learning which were absent in AD animals that were not exposed to the light-dark variations as well as in normal mice with jet lag.
Follow-up tissue analysis results revealed that jet lag lowered the levels of glutathione, an important antioxidant that prevents damage to key cellular components caused by reactive oxygen species, in brain cells of all mice; however, these levels were much lower in AD mouse models and related to poor performance in the water maze tests. Deficiencies in glutathione are responsible for redox alterations in brain cells, which leads to alterations in the oxidation state of atoms and may affect brain inflammation and metabolism.
Brewer pointed to the accelerated oxidative stress as a vital component in Alzheimer’s-related learning and memory loss and noted that potential drug treatments could target these changes in redox reactions. “This study suggests that clinicians and caregivers should add good sleep habits to regular exercise and a healthy diet to maximize good memory,” he said.