Results suggest greater
emphasis on managing slumber habits of people with AD risk
Newswise, October 29, 2015 — Chemical changes in brain cells
caused by disturbances in the body’s day-night cycle may be a key underlying
cause of the learning and memory loss associated with Alzheimer’s disease,
according to a University of California, Irvine study.
The research on mice, led by UCI biomedical engineering
professor Gregory Brewer, provides the first evidence that circadian
rhythm-altering sleep disruptions similar to jet lag promote memory problems
and chemical alterations in the brain.
Clinical application of this finding may lead to more emphasis
on managing the sleep habits of people at risk for Alzheimer’s disease and
those with mild cognitive impairment. Study results appear online in the
Journal of Alzheimer’s Disease.
People with Alzheimer’s often have problems with sleeping or
may experience changes in their slumber schedule. Scientists do not completely
understand why these disturbances occur.
“The issue is whether poor sleep accelerates the development
of Alzheimer’s disease or vice versa,” said Brewer, who’s affiliated with UCI’s
Institute for Memory Impairments and Neurological Disorders. “It’s a
chicken-or-egg dilemma, but our research points to disruption of sleep as the
accelerator of memory loss.”
In order to examine the link between learning and memory and
circadian disturbances, his team altered normal light-dark patterns with an
eight-hour shortening of the dark period every three days for young mouse
models of Alzheimer’s disease and normal mice.
The resulting jet lag greatly reduced activity in both sets of
mice, and the researchers found that in water maze tests, the AD mouse models
had significant learning impairments absent in the AD mouse models not exposed
to light-dark variations and in normal mice with jet lag.
In follow-up tissue studies, they saw that jet lag caused a
decrease in glutathione levels in the brain cells of all the mice. But these
levels were much lower in the AD mouse models and corresponded to poor
performance in the water maze tests. Glutathione is a major antioxidant that
helps prevent damage to essential cellular components.
Glutathione deficiencies produce redox changes in brain cells.
Redox reactions involve the transfer of electrons, which leads to alterations
in the oxidation state of atoms and may affect brain metabolism and
inflammation.
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.
Kelsey LeVault and Shelley Tischkau of the Southern Illinois
University School of Medicine contributed to the research, which received
support from the National Institutes of Health (grant R01 AG032431).
About the University of California, Irvine: Currently
celebrating its 50th anniversary, UCI is the youngest member of the prestigious
Association of American Universities. The campus has produced three Nobel
laureates and is known for its academic achievement, premier research,
innovation and anteater mascot.
Led by Chancellor Howard Gillman, UCI has more than 30,000
students and offers 192 degree programs. It’s located in one of the world’s
safest and most economically vibrant communities and is Orange County’s
second-largest employer, contributing $4.8 billion annually to the local
economy. For more on UCI, visit www.uci.edu.
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