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Controlling Hypertension Now May Keep Alzheimer's Away Later in Life

January 18, 2013

A recently-completed US study, the results of which were published in the Journal of the American Medical Association Neurology , showed a connection between controlling or preventing hypertension and other risk factors earlier in life and limiting the damaging brain changes caused by age-related neurological diseases including Alzheimer's.

A recently-completed US study, the results of which were published in the Journal of the American Medical Association Neurology , showed a connection between controlling or preventing hypertension and other risk factors earlier in life  and limiting the damaging brain changes caused by age-related neurological diseases including Alzheimer's.

The accumulation of plaque in the brain – widely considered the first Alzheimer’s symptom – begins years before a patient begins experiencing memory problems. About one in five people carry the ApoE4 gene linked to the accumulation of deposits of amyloid protein plaque.

The study participants, ranging in age from 30 to 89, were grouped by their hypertension status (those taking medication to control hypertension, those with hypertension not taking medication, and patients with normal blood pressure). Each group was sub-classified based on whether they carried the ApoE4 allele, the genetic variation associated with dementia.

 
 
 
Those not taking medication to control their high blood pressure who had the genetic risk factor had significantly higher amyloid levels compared to all other participants. Among hypertensive patients whose condition was being controlled through medication, the study showed that even those with the genetic risk factor had amyloid plaque levels no worse than non-hypertensive patients without the genetic risk factor.

The study provides encouraging data that the long term benefits of controlling high blood pressure may extend beyond reduced risk of stroke and other cardiovascular problems to also include a reduced Alzheimer’s risk.


Missing DNA linked to early-onset Parkinson's disease
Research scientists have discovered a previously-unknown link between a missing piece of DNA and developing early-onset Parkinson's disease. The link was discovered as part of a research study being conducted by scientists from the Centre for Addiction and Mental Health and the University Health Network in Canada.

 
 
 
 
The study of adults age 35 to 64 who were missing DNA from a particular area of chromosome 22 (termed 22q11.2 deletion syndrome) revealed a significantly higher prevalence of Parkinson's disease in the group compared to expected rates among the general population of similarly-aged adults.

While most adults with 22q11.2 deletion syndrome don’t go on to develop Parkinson’s disease, the research team that made the discovery suggested that clinical genetic testing be considered for those with the syndrome, as testing offers an earlier opportunity to ensure those patients found to have Parkinson’s can receive the best possible care.

 

Trouble sleeping may be early Alzheimer’s symptom

The findings of a new study published in Proceedings  of the National Academy of Science suggest that sleep loss may be an early sign of Alzheimer's disease. 

Sleep problems are relatively common among Alzheimer’s patients. Studies conducted on laboratory animals found sleep loss was correlated to the build-up of amyloid protein plaque in the brain.
 
And other research suggests a cause/effect connection between sleep and Alzheimer’s: Changes to the brain due to Alzheimer’s may make it more difficult to sleep, while lack of sleep may contribute to those types of brain changes.

The latest study involved 145 adults from 45 to 75 with no signs of dementia or memory problems. Spinal fluid testing showed one in five carried pre-Alzheimer’s markers.

 
 
Participants kept daily sleep and napping diaries while a wrist sensor tracked daily activity. Those with pre-Alzheimer’s markers had an 80% sleep efficiency versus 84% for those who didn’t have the markers. Each group spent the same amount of time in bed, but the pre-Alzheimer’s group didn’t sleep as long and napped more frequently.

There are many possible factors that can cause sleep problems. Many of them are not believed to lead to Alzheimer’s.
 
 
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