Potential link between sleep and Alzheimer's is intriguing
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Poor sleep linked to cortical amyloid burden

MINNEAPOLIS – People who report feeling more sleepy and less rested have elevated levels of amyloid in regions of the brain commonly involved in Alzheimer’s disease, according to a cohort study presented at the annual meeting of the Associated Professional Sleep Societies.

Researchers studied 98 asymptomatic, cognitively healthy late- to middle-age adults from the WRAP (Wisconsin Registry for Alzheimer’s Prevention) program, the majority of whom were at elevated risk for the disease because of family history.

Dr. Kate Sprecher

Self-reported somnolence, poorer sleep quality, and sleep problems were significantly correlated with higher levels of amyloid deposition in the cortex overall and in four subregions typically affected in Alzheimer’s disease.

"It does appear that there is an association between amyloid burden and sleepiness, and that relationship is present in adults who are cognitively healthy but who are at risk of developing Alzheimer’s disease in the future. They are fairly young in terms of amyloid pathology," said first author Kate Sprecher, a PhD candidate in the neuroscience training program at the University of Wisconsin–Madison. She acknowledged that the findings may differ in a cohort not enriched for people at elevated risk.

"We can’t say from these data whether sleep is driving amyloid deposition or whether amyloid deposition is disrupting sleep," she said. "Nonetheless, it’s kind of tantalizing that sleep may be a tool that we can use to prevent or delay Alzheimer’s pathology. We may be able to intervene early in the disease, when people are actually able to respond to treatment, because typically, current drugs are targeting later disease, when a great deal of neurodegeneration has already taken place. So sleep may be something that we can target really early."

 

 

The researchers plan to investigate the observed association using objective measures of sleep and obstructive sleep apnea (OSA), according to Ms. Sprecher. "And we’ll do some longitudinal follow-up as well in our cohort to see how sleep changes might relate to actual progression of the disease."

Study participants completed the Medical Outcomes Study (MOS) Sleep Scale and the Epworth Sleepiness Scale (ESS). Amyloid deposition in the brain was measured by positron-emission tomography performed with Pittsburgh Compound B.

The participants were 63 years old, on average, and two-thirds were female. Overall, 76% had a family history of Alzheimer’s, and 34% were positive for the APOE4 allele, which is associated with risk of this disease.

‘It’s kind of tantalizing that sleep may be a tool that we can use to prevent or delay Alzheimer’s pathology.’

Analyses adjusted for these and other confounders showed a correlation (P less than or equal to .05) between somnolence on the MOS Sleep Scale – the average of scores for drowsiness, trouble staying awake, and napping – and the burden of amyloid in the left supramarginal gyrus (correlation [r] = 0.22), the left frontal medial orbital cortex (r = 0.21), and the left frontal inferior orbital cortex (r = 0.21).

Poorer quality of sleep was significantly correlated with amyloid burden in the cortex overall (r = 0.25) as well as in the left and right precuneus (r = 0.23 and 0.25), the right supramarginal gyrus (r = 0.23), the left and right frontal medial orbital cortex (r = 0.29 and 0.29), and the left and right frontal inferior orbital cortex (r = 0.26 and 0.25). Scores on the Sleep Problem Index were also linked to greater burden in some of these cortical areas.

Although ESS scores were significantly correlated with MOS scores, they were not directly correlated with amyloid burden in any of the regions studied. "This could be because the two questionnaires probe slightly different aspects of sleepiness," Ms. Sprecher said in an interview. "The ESS asks how likely you are to fall asleep in several common situations such as while watching TV or driving a car. The MOS asks whether you take naps, feel sleepy during the day, or feel that you get enough sleep at night. Therefore, the MOS may be better at probing how adequate your sleep is, even if you are managing to stay awake during the day."

Ms. Sprecher had no disclosures.

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Dr. Vera DePalo, FCCP, comments: As we learn more about the benefits of healthy sleep, we begin to recognize how integral sleep is to maintaining a healthy, well-functioning body.

The work described in this article is intriguing.

It provides a potential first point of recognition for a link between the poor sleep and the pathologic findings seen in those individuals who are at risk for Alzheimer’s disease.

While it was the subjective sleep scale used to assess sleepiness in the work described which correlated with amyloid deposition, it will be very interesting to see if the objective measures of impaired sleep correlate as well.

More study is needed to better understand the potential link. 

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Body

Dr. Vera DePalo, FCCP, comments: As we learn more about the benefits of healthy sleep, we begin to recognize how integral sleep is to maintaining a healthy, well-functioning body.

The work described in this article is intriguing.

It provides a potential first point of recognition for a link between the poor sleep and the pathologic findings seen in those individuals who are at risk for Alzheimer’s disease.

While it was the subjective sleep scale used to assess sleepiness in the work described which correlated with amyloid deposition, it will be very interesting to see if the objective measures of impaired sleep correlate as well.

More study is needed to better understand the potential link. 

Body

Dr. Vera DePalo, FCCP, comments: As we learn more about the benefits of healthy sleep, we begin to recognize how integral sleep is to maintaining a healthy, well-functioning body.

The work described in this article is intriguing.

It provides a potential first point of recognition for a link between the poor sleep and the pathologic findings seen in those individuals who are at risk for Alzheimer’s disease.

While it was the subjective sleep scale used to assess sleepiness in the work described which correlated with amyloid deposition, it will be very interesting to see if the objective measures of impaired sleep correlate as well.

More study is needed to better understand the potential link. 

Title
Potential link between sleep and Alzheimer's is intriguing
Potential link between sleep and Alzheimer's is intriguing

MINNEAPOLIS – People who report feeling more sleepy and less rested have elevated levels of amyloid in regions of the brain commonly involved in Alzheimer’s disease, according to a cohort study presented at the annual meeting of the Associated Professional Sleep Societies.

Researchers studied 98 asymptomatic, cognitively healthy late- to middle-age adults from the WRAP (Wisconsin Registry for Alzheimer’s Prevention) program, the majority of whom were at elevated risk for the disease because of family history.

Dr. Kate Sprecher

Self-reported somnolence, poorer sleep quality, and sleep problems were significantly correlated with higher levels of amyloid deposition in the cortex overall and in four subregions typically affected in Alzheimer’s disease.

"It does appear that there is an association between amyloid burden and sleepiness, and that relationship is present in adults who are cognitively healthy but who are at risk of developing Alzheimer’s disease in the future. They are fairly young in terms of amyloid pathology," said first author Kate Sprecher, a PhD candidate in the neuroscience training program at the University of Wisconsin–Madison. She acknowledged that the findings may differ in a cohort not enriched for people at elevated risk.

"We can’t say from these data whether sleep is driving amyloid deposition or whether amyloid deposition is disrupting sleep," she said. "Nonetheless, it’s kind of tantalizing that sleep may be a tool that we can use to prevent or delay Alzheimer’s pathology. We may be able to intervene early in the disease, when people are actually able to respond to treatment, because typically, current drugs are targeting later disease, when a great deal of neurodegeneration has already taken place. So sleep may be something that we can target really early."

 

 

The researchers plan to investigate the observed association using objective measures of sleep and obstructive sleep apnea (OSA), according to Ms. Sprecher. "And we’ll do some longitudinal follow-up as well in our cohort to see how sleep changes might relate to actual progression of the disease."

Study participants completed the Medical Outcomes Study (MOS) Sleep Scale and the Epworth Sleepiness Scale (ESS). Amyloid deposition in the brain was measured by positron-emission tomography performed with Pittsburgh Compound B.

The participants were 63 years old, on average, and two-thirds were female. Overall, 76% had a family history of Alzheimer’s, and 34% were positive for the APOE4 allele, which is associated with risk of this disease.

‘It’s kind of tantalizing that sleep may be a tool that we can use to prevent or delay Alzheimer’s pathology.’

Analyses adjusted for these and other confounders showed a correlation (P less than or equal to .05) between somnolence on the MOS Sleep Scale – the average of scores for drowsiness, trouble staying awake, and napping – and the burden of amyloid in the left supramarginal gyrus (correlation [r] = 0.22), the left frontal medial orbital cortex (r = 0.21), and the left frontal inferior orbital cortex (r = 0.21).

Poorer quality of sleep was significantly correlated with amyloid burden in the cortex overall (r = 0.25) as well as in the left and right precuneus (r = 0.23 and 0.25), the right supramarginal gyrus (r = 0.23), the left and right frontal medial orbital cortex (r = 0.29 and 0.29), and the left and right frontal inferior orbital cortex (r = 0.26 and 0.25). Scores on the Sleep Problem Index were also linked to greater burden in some of these cortical areas.

Although ESS scores were significantly correlated with MOS scores, they were not directly correlated with amyloid burden in any of the regions studied. "This could be because the two questionnaires probe slightly different aspects of sleepiness," Ms. Sprecher said in an interview. "The ESS asks how likely you are to fall asleep in several common situations such as while watching TV or driving a car. The MOS asks whether you take naps, feel sleepy during the day, or feel that you get enough sleep at night. Therefore, the MOS may be better at probing how adequate your sleep is, even if you are managing to stay awake during the day."

Ms. Sprecher had no disclosures.

MINNEAPOLIS – People who report feeling more sleepy and less rested have elevated levels of amyloid in regions of the brain commonly involved in Alzheimer’s disease, according to a cohort study presented at the annual meeting of the Associated Professional Sleep Societies.

Researchers studied 98 asymptomatic, cognitively healthy late- to middle-age adults from the WRAP (Wisconsin Registry for Alzheimer’s Prevention) program, the majority of whom were at elevated risk for the disease because of family history.

Dr. Kate Sprecher

Self-reported somnolence, poorer sleep quality, and sleep problems were significantly correlated with higher levels of amyloid deposition in the cortex overall and in four subregions typically affected in Alzheimer’s disease.

"It does appear that there is an association between amyloid burden and sleepiness, and that relationship is present in adults who are cognitively healthy but who are at risk of developing Alzheimer’s disease in the future. They are fairly young in terms of amyloid pathology," said first author Kate Sprecher, a PhD candidate in the neuroscience training program at the University of Wisconsin–Madison. She acknowledged that the findings may differ in a cohort not enriched for people at elevated risk.

"We can’t say from these data whether sleep is driving amyloid deposition or whether amyloid deposition is disrupting sleep," she said. "Nonetheless, it’s kind of tantalizing that sleep may be a tool that we can use to prevent or delay Alzheimer’s pathology. We may be able to intervene early in the disease, when people are actually able to respond to treatment, because typically, current drugs are targeting later disease, when a great deal of neurodegeneration has already taken place. So sleep may be something that we can target really early."

 

 

The researchers plan to investigate the observed association using objective measures of sleep and obstructive sleep apnea (OSA), according to Ms. Sprecher. "And we’ll do some longitudinal follow-up as well in our cohort to see how sleep changes might relate to actual progression of the disease."

Study participants completed the Medical Outcomes Study (MOS) Sleep Scale and the Epworth Sleepiness Scale (ESS). Amyloid deposition in the brain was measured by positron-emission tomography performed with Pittsburgh Compound B.

The participants were 63 years old, on average, and two-thirds were female. Overall, 76% had a family history of Alzheimer’s, and 34% were positive for the APOE4 allele, which is associated with risk of this disease.

‘It’s kind of tantalizing that sleep may be a tool that we can use to prevent or delay Alzheimer’s pathology.’

Analyses adjusted for these and other confounders showed a correlation (P less than or equal to .05) between somnolence on the MOS Sleep Scale – the average of scores for drowsiness, trouble staying awake, and napping – and the burden of amyloid in the left supramarginal gyrus (correlation [r] = 0.22), the left frontal medial orbital cortex (r = 0.21), and the left frontal inferior orbital cortex (r = 0.21).

Poorer quality of sleep was significantly correlated with amyloid burden in the cortex overall (r = 0.25) as well as in the left and right precuneus (r = 0.23 and 0.25), the right supramarginal gyrus (r = 0.23), the left and right frontal medial orbital cortex (r = 0.29 and 0.29), and the left and right frontal inferior orbital cortex (r = 0.26 and 0.25). Scores on the Sleep Problem Index were also linked to greater burden in some of these cortical areas.

Although ESS scores were significantly correlated with MOS scores, they were not directly correlated with amyloid burden in any of the regions studied. "This could be because the two questionnaires probe slightly different aspects of sleepiness," Ms. Sprecher said in an interview. "The ESS asks how likely you are to fall asleep in several common situations such as while watching TV or driving a car. The MOS asks whether you take naps, feel sleepy during the day, or feel that you get enough sleep at night. Therefore, the MOS may be better at probing how adequate your sleep is, even if you are managing to stay awake during the day."

Ms. Sprecher had no disclosures.

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Key clinical point: Improved sleep quality might provide protection from Alzheimer’s disease.

Major finding: Self-reported somnolence, poorer sleep quality, and sleep problems were associated with greater amyloid burden in areas of the brain known to be affected by Alzheimer’s disease (P less than .05).

Data source: A cohort study of 98 asymptomatic, cognitively healthy late middle-age adults, the majority at elevated risk for Alzheimer’s disease.

Disclosures: Ms. Sprecher disclosed no relevant conflicts of interest.