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Alzheimer's disease: Scientists discover how a ROGUE protein triggers the brain disease

07 July 2017

In addition to answering questions about their quality of sleep, subjects provided spinal-fluid samples for analysis. In Alzheimer's disease there are two types of abnormal proteins or neurofibrillary lesions as they are termed, in the brain.

Amyloid plaques develop in parts of the brain that play a role in visual recognition and memory, causing symptoms of the disorder.

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".

Researchers point out that disrupted sleep or lack of sleep may lead to amyloid plaque build-up because the clearance mechanism of the brain kicks into action only while sleeping. Not only drug development in these diseases, it could also help us understand the disease more clearly.

All participants had known risk factors for Alzheimer's, such as family history or evidence of the APOE gene, which is associated with a greater risk of the disease.

Lead scientist Dr Barbara Bendlin, from the University of Wisconsin-Madison in the U.S., said: "Previous evidence has shown that sleep may influence the development or progression of Alzheimer's disease in various ways". While tau filaments are formed within the nerve cells of the brain, beta amyloid proteins are formed outside the nerve cells in the form of filaments.

The results of the small study hint that people with a higher-than-normal risk of Alzheimer's disease who had worse sleep quality, more sleep problems and daytime sleepiness had more markers for Alzheimer's disease in their spinal fluid than those who didn't have sleep issues.

'Our study looked not only for amyloid but for other biological markers in the spinal fluid as well.

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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".

'Our findings demonstrate that the relationship between sleep and Alzheimer's disease is present in late midlife in the absence of cognitive impairment.

Participants were surveyed about sleep quality.

"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".

"Amyloid structures can form in many different ways, so it has been unclear how close these lab versions resembled those in human disease".

Finding out what causes Alzheimer's could be critical to stopping the disease as early as possible, before irreversible damage has been done.

"We're looking at groups of people, and over the whole group we find the association of poor sleep with the markers of Alzheimer's", said Bendlin. As the mice slept, their brains actually changed shape, expanding to allow them to better flush out these toxins that had built up during the day, The Huffington Post reported.

Alzheimer's disease: Scientists discover how a ROGUE protein triggers the brain disease