Poor sleep may point to onset of Alzheimers disease

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Each person was asked to complete sleep assessments and had their cerebrospinal fluid collected.

A new study in Neurology, the journal for the American Academy of Neurology, is adding to that research by looking at the relationship between sleep quality and levels of various proteins and inflammatory markers in the cerebrospinal fluid of 101 cognitively healthy adults with an average age of 63. Without sufficient time to self-clean, brain toxins that may lead to Alzheimer's disease have time to build up.

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Dr James Pickett, head of research at the charity Alzheimer's Society, said: "Tau protein, one of the hallmarks of Alzheimer's disease, has never been seen in this level of detail before".

It's possible changes in the brain associated with Alzheimer's could affect sleep, as opposed to the other way around, Bendlin added. "This new work will help to develop better compounds for diagnosing and treating Alzheimer's and other diseases which involve defective Tau". Those participants suffering from daytime drowsiness, and those who reported poor quality of sleep, had more biological markers for the disease than those who did not report sleep problems.

They either had a parent with the disease or were a carrier of a gene that increases the risk for Alzheimers disease called apolipoprotein E or APOE.

Biological markers included signs of amyloid, tau and brain cell damage and inflammation.

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Fellow senior author Dr Michel Goedert, who also worked on the original research 30 years ago, said: "We have known for nearly three decades that the abnormal assembly of Tau protein into filaments is a defining characteristic of Alzheimer's disease".

For example, there was no link between biological markers in the spinal fluid and the disease sleep apnea, a disorder causing breathing problems during sleep.

A limitation of the Wisconsin-Madison study is that subjects' reports of sleep quality are subject to error.

"It's important to identify modifiable risk factors for Alzheimer's given that estimates suggest that delaying the onset of Alzheimer's disease in people by a mere five years could reduce the number of cases we see in the next 30 years by 5.7 million and save US$367 billion (AU$480 billion) in health care spending".

While there's no shortage of research examining how abnormal tau and amyloid beta proteins function, it's been unclear just how much artificial samples assembled in the lab differ from the structures that form in the lab.

Future studies may require people to attend sleep laboratories so their bedtime habits can be monitored, according to the researchers.

One thing that could have thrown the findings off is that the participants reported their own sleep problems.