Are sleep problems a key factor in Alzheimer’s?

October, 2012

A mouse study shows that sleep deprivation and aggregation of amyloid beta go hand in hand, and may be key players on the road to Alzheimer’s.

I reported a few months ago on some evidence of a link between disturbed sleep and the development of Alzheimer’s. Now a mouse study adds to this evidence.

The mouse study follows on from an earlier study showing that brain levels of amyloid beta naturally rise when healthy young mice are awake and drop after they go to sleep, and that sleep deprivation disrupted this cycle and accelerated the development of amyloid plaques. This natural rhythm was confirmed in humans.

In the new study, it was found that this circadian rhythm showed the first signs of disruption as soon as Alzheimer’s plaques began forming in the mice’s brains. When the genetically engineered mice were given a vaccine against amyloid beta, the mice didn’t develop plaques in old age, the natural fluctuations in amyloid beta levels continued, and sleep patterns remained normal.

Research with humans in now underway to see whether patients with early markers of Alzheimer’s show sleep problems, and what the nature of these problems is.

Just to make it clear: the point is not so much that Alzheimer’s patients are more likely to have sleep problems, but that the sleep problems may in fact be part of the cause of Alzheimer’s disease development. The big question, of course, is whether you can prevent its development by attacking the dysfunction in circadian rhythm. (See more on this debate at Biomed)

Reference: 

Related News

A study involving 254 people with dementia living at home has found that 99% of people with dementia and 97% of their caregivers had one or more unmet needs, 90% of which were safety-related.

A new U.S. study suggests that Alzheimer's disease and other dementias are markedly under-reported on death certificates and medical records. Death certificates tend to only provide an immediate cause, such as pneumonia, and don’t mention the underlying condition that provoked it.

It’s often argued that telling people that they carry genes increasing their risk of Alzheimer’s will simply upset them to no purpose. A new study challenges that idea.

11 new genetic susceptibility factors for Alzheimer’s identified

Understanding a protein's role in familial Alzheimer's disease

Analysis of data from 237 patients with mild cognitive impairment (mean age 79.9) has found that, compared to those carrying the ‘normal’ ApoE3 gene (the most common variant of the ApoE gene), the ApoE4 carriers showed markedly greater rates of shrinkage in 13 of 15 brain regions thought to be k

Analysis of data from more than 8,000 people, most of them older than 60, has revealed that, among the 5,000 people initially tested cognitively normal, carrying one copy of the “Alzheimer’s gene” (ApoE4) only slightly increased men’s risk of developing

Analysis of 700 subjects from the Alzheimer's Disease Neuroimaging Initiative has revealed a genetic mutation (rs4728029) that’s associated with people who develop Alzheimer’s pathology but don’t show clinical symptoms in their lifetime.

Analysis of brain scans and cognitive scores of 64 older adults from the NIA's Baltimore Longitudinal Study of Aging (average age 76) has found that, between the most cognitively stable and the most declining (over a 12-year period), there was no significant difference in the total amount of amy

A pilot study involving 94 older adults, of whom 18 had Alzheimer’s, 24 had

Pages

Subscribe to Latest newsSubscribe to Latest newsSubscribe to Latest health newsSubscribe to Latest news