Sound sleep can reduce Alzheimer’s risk
A new study shows that sound sleep substantially offsets the negative effect of the most common genetic risk factor for Alzheimer's disease (AD).
"These findings highlight a thus far unappreciated biological and clinical link between sleep, genetics, brain pathology, cognition and dementia risk," says Dr. Andrew Lim, principal author of the study and a sleep neurologist at Sunnybrook. "Approximately 10 to 20 per cent of the general population carries the risk variant of the APOE gene, putting them at a substantially elevated (25-40%) lifetime risk of developing AD. Our results suggest that by assessing sleep in these individuals, we may be able to identify who among them is at highest risk for developing AD. Moreover, they raise the possibility that we may be able to intervene to reduce that risk by improving sleep."
The study followed 698 older adults who were participating in the Memory and Aging project, an ongoing large-scale study of aging and AD risk factors. Participants did not have dementia at the outset of the study and had annual evaluation for AD during a follow-up period of up to six years.
Over the six-year period, 98 individuals developed AD. Better sleep not only weakened the effect of the APOE gene on the risk of incident AD, but also lessened the effect of the gene on the annual rate of cognitive decline. Moreover, it also lessened the impact of this gene on the burden of neurofibrillary tangles, a key mechanism leading to AD, in the brains of those who passed away during the follow-up period.
"A combination of genetic, behavioural, and environmental factors contributes to the risk of AD in elderly people, and although we cannot as of now alter a person's genes, there are many social, environmental and medical contributors to poor sleep that are modifiable and that may help to reduce that risk," adds Dr. Lim.
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Consolidating sleep can reduce risk of Alzheimer's
A new study shows that sound sleep substantially offsets the negative effect of the most common genetic risk factor for Alzheimer's disease (AD).
"These findings highlight a thus far unappreciated biological and clinical link between sleep, genetics, brain pathology, cognition and dementia risk," says Dr. Andrew Lim, principal author of the study and a sleep neurologist at Sunnybrook Health Sciences Centre. "Approximately 10 to 20 per cent of the general population carries the risk variant of the APOE gene, putting them at a substantially elevated (25-40%) lifetime risk of developing AD. Our results suggest that by assessing sleep in these individuals, we may be able to identify who among them is at highest risk for developing AD. Moreover, they raise the possibility that we may be able to intervene to reduce that risk by improving sleep."
Published online in the October 21 issue of JAMA Neurology, the study followed 698 older adults who were participating in the Memory and Aging project, an ongoing large-scale study of aging and AD risk factors. Participants did not have dementia at the outset of the study and had annual evaluation for AD during a follow-up period of up to six years.
Over the six-year period, 98 individuals developed AD. Better sleep not only weakened the effect of the APOE gene on the risk of incident AD, but also lessened the effect of the gene on the annual rate of cognitive decline. Moreover, it also lessened the impact of this gene on the burden of neurofibrillary tangles, a key mechanism leading to AD, in the brains of those who passed away during the follow-up period.
The authors hypothesized that better sleep may protect against biological mechanisms linking the APOE gene to the formation of neurofibrillary tanglesand that interventions to improve sleep consolidation may be a useful approach to prevent the development of these tangles and therefore reduce the risk of AD in individuals with the risk variant of the APOE gene.
"A combination of genetic, behavioural, and environmental factors contributes to the risk of AD in elderly people, and although we cannot as of now alter a person's genes, there are many social, environmental and medical contributors to poor sleep that are modifiable and that may help to reduce that risk," adds Dr. Lim, also an assistant professor at University of Toronto.
These results add to the growing body of evidence supporting a link between sleep, genetic susceptibility, and AD pathology. Future interventional studies will help to further define the appropriate role for genotyping, sleep assessment, and sleep interventions in the clinical management of individuals at risk for AD.
Co-authors on the study include Dr. Lei Yu (Rush Alzheimer's Disease Center), Dr. Matthew Kowgier (University of Toronto), Dr. Julie Schneider (Rush Alzheimer's Disease Center), Dr. Aron Buchman (Rush Alzheimer's Disease Centre), and Dr. David Bennett (Rush Alzheimer's Disease Center).
The Memory and Aging Project is supported by grants from the National Institutes of Health. Dr. Lim is supported by grants from the Canadian Institutes of Health Research and the Heart and Stroke Foundation of Ontario.
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