Two Studies Find Promising New Ways to Detect Alzheimer’s Earlier

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Sleep patterns and markers in spinal fluid may hint at the first signs of the neurodegenerative disorder.

The Centers for Disease Control and Prevention estimates that 5 million Americans have Alzheimer’s disease, and while there are no effective treatments, experts believe detecting the disease early can help patients to strengthen memory and cognitive functions and potentially slow down the buildup of brain plaques that are the hallmark of the condition. Two studies, both published in the Journal of the American Medical Association, hint at potentially encouraging ways to identify those who might be at risk, at the earliest possible stages of the disease.

(MORE: Study Shows Alzheimer’s Protein May Not Spread Like a Virus)

In one study from the Washington University School of Medicine in St. Louis, researchers found that levels of the protein amyloid, which makes up these plaques, were correlated with poor sleep quality. Previous studies in animals showed that animals that slept less tended to develop more plaques, but it wasn’t clear whether poor sleep can contribute to the formation of amyloid plaques, or whether the buildup of these deposits causes disturbances in sleep.

To study the connection further, the scientists asked 145 cognitively normal individuals aged 45 to 75, who were enrolled at the Alzheimer’s disease research center, to keep a diary of their sleep patterns for two weeks. The volunteers recorded when they went to bed, when they woke up in the morning, how many naps they took and whether they felt sleepy during the day. The scientists had the advantage of already having samples of the participants’ spinal fluid, so they could also match up the sleep records with the level of amyloid protein in the brain of each patient.

All of the participants slept about the same amount, but there were stark differences in the quality of that sleep. Thirty-two participants showed higher levels of amyloid buildup that was classified as preclinical Alzheimer’s disease and also had worse sleep quality. These volunteers were less likely to spend time their time in bed in restful, deep sleep than those with lower levels of amyloid.

(MORE: New Research on Understanding Alzheimer’s)

Because none of the participants were experiencing any symptoms of Alzheimer’s, the researchers believe such sleep disturbances may be among the earliest signs of the disease, and could help to identify those at risk of developing Alzheimer’s. It’s still possible that the link between poor sleep and Alzheimer’s disease works both ways and that amyloid buildup could interfere with neurological sleep functions at the same time that restless sleep creates conditions promoting the deposit of the amyloid protein.

Either way, the scientists believe sleep disturbances could not only help in identifying the most vulnerable populations but aid in the testing of new treatments. Measuring the effect that novel drugs or therapies have in improving sleep quality and lowering amyloid levels could serve as a marker for their effectiveness. “Sleep measures themselves could be used as markers of brain function, thereby facilitating faster and easier clinical trials of promising treatments in the preclinical and early clinical stages of Alzheimer’s disease,” the authors write.

(MORE: Is Alzheimer’s Caused by Contagious Proteins?)

In the second study, researchers from the University of Minnesota focused more specifically on which markers of amyloid were the best representatives of the protein’s buildup in the brain. They studied spinal fluid from 107 adults, about half of whom showed signs of Alzheimer’s or cognitive impairment and half of whom did not. They then compared their results with those of 10 younger and cognitively normal controls to ensure that they were zeroing in on the most reliable markers for Alzheimer’s.

(MORE: Use It or Lose It: Keeping Brain Active May Help Ward Off Alzheimer’s)

For years now, scientists have known that the amyloid protein that builds up in the neurodegenerative condition actually comes from a larger protein that is broken down into various fragments. So the Minnesota researchers concentrated on two of these, the beta-amyloid trimers and beta-amyloid*56. They found that levels of these fragments were elevated among participants who already showed symptoms of Alzheimer’s, but were lower among those who didn’t have the symptoms and among the younger controls. Levels of these compounds also increased with age, suggesting that they serve as a viable target for new treatments as well, since eliminating or hampering their aggregation might hold off some of the symptoms of Alzheimer’s.

(MORE: Scientists Identify Rare Gene Mutation That Protects Against Alzheimer’s)

Both methods require additional confirmation, but as experts learn more about the processes that drive Alzheimer’s, they hope to find more interventions that can reduce the severity of the disease or, ultimately, prevent it altogether.


Excellent article! The role of sleep in neuro-immune disorders like fibromyalgia, for example, are pretty much overlooked by the average physician. Poor quality sleep is one of the key characteristics of chronic fatigue syndrome and fibromyalgia; however, the medical community is reluctant to treat these conditions with sleep medications. Delaying the use of sleep medication to treat this condition leads to more disability and poorer quality of life among those who suffer from these poorly understood conditions.

The research you report on highlights the need to conduct longitudinal studies with those who have fibromyalgia to determine whether they are at increased risk of developing Alzheimer's disease later in life. We need research agencies to focus their efforts on this type of research instead on the personality traits of those who suffer from mysterious and highly stigmatizing conditions. MS was a psychosomatic illness not long ago, and I believe that in the next couple of decades we'll have robust evidence to suggest that fibromyalgia is a much more serious condition than the medical community suggests.


Thank you to Time for covering this research, and congratulations to Dr. David Holtzman, senior author of this study, and a member of BrightFocus’ Alzheimer's Disease Research Scientific Review Committee.  This report makes the difficult bridge between familiar human behaviors and the molecular reasons for Alzheimer's disease. The Alzheimer's research community is moving closer to finding new treatments to forestall the effects of the disease because of leading researchers like David Holtzman.

Guy Eakin, PhD

Vice President of Scientific Affairs

BrightFocus Foundation


Interesting overview. One small detail though: The amyloid trimers and *56 are not different fragments from the longer protein (APP) than the amyloid beta peptides: they are aggregation-forms containing only amyloid beta  (trimers = three amyloid beta peptides, also *56 is thought to contain multiple amyloid-beta peptides). All the same breakdown product.