Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Wednesday, September 19, 2018

Daytime sleepiness found to be a potential risk factor for Alzheimer’s disease

Then your doctor needs to find out EXACTLY what is causing post stroke fatigue and prevent it from occurring. Or is your doctor doing NOTHING because they are waiting for SOMEONE ELSE TO SOLVE THE PROBLEM? 

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.

3. A 20% chance in this research.   July 2013.


But looking at the title it refers to cognitively normal so it wouldn't apply to us with our lost 5 cognitive years from your stroke? Or does it apply? Stroke survivors demand answers. 
Daytime sleepiness found to be a potential risk factor for Alzheimer’s disease 
A recent study has reported that older adults who frequently report feeling sleepy during the day are three times more likely to develop beta-amyloid deposits in later life.
Beta-amyloid is a protein which is characteristically seen Alzheimer’s disease (AD). The findings are important because they suggest that helping people to get a good night’s sleep could prevent AD.
Woman sleeping during the day at her deskImage Credit: fizkes / Shutterstock
Previous research has already shown that AD risk could be reduced by modifying diet, exercise and cognitive activity.
However, sleep has not so far been found to be a risk factor, despite disturbed sleep being a hallmark of the disease.
It is thought that disturbed sleep patterns in patients with AD could be due to the growth of the amyloid plaques and resulting neuronal changes.
The long-term study was based on data acquired from the Baltimore Longitudinal Study of Aging (BLSA) that was initiated in 1958 by the National Institute on Aging (NIA).
The study was designed to monitor the long-term health of thousands of volunteers in order to discover risk factors for age-related conditions.
One of the components of this monitoring was a periodic questionnaire (from 1991 to 2000) which contained the questions: “Do you often become drowsy or fall asleep during the daytime when you wish to be awake?” and “Do you nap?”.
The first question required a yes/no response, while the second could be answered by “daily,” “1-2 times/week,” “3-5 times/week,” and “rarely or never.”
A smaller group of volunteers in this study began to undergo neuroimaging examinations in  1994, and some of them had PET (positron emission tomography) scans from 2005 onwards.
These scans used the radioactive Pittsburgh compound B (PIB) to pick up beta-amyloid deposits in the brain.
In total, 123 volunteers provided answers to the questions and also had a PET scan (after 16 years, on average).
Analysis of the data from this subgroup showed that those who answered “Yes” to daytime sleepiness had an unadjusted risk of beta-amyloid deposits which was three times greater than in those who answered “No”.
When the data was adjusted for factors such as age, sex, education and body-mass index which could affect daytime sleepiness, the risk still remained 2.75 times higher in the first group. This finding increases the possibility that AD could in part be caused by nighttime sleep disturbances.
Volunteers who reported napping in the daytime also had a higher unadjusted risk, about twice as high, but this was not statistically significant.
The reason for this correlation is not known but could be due to the plaque-forming activity of daytime sleepiness itself.
The researchers also pointed out that the amyloid protein itself could conceivably be the cause of the daytime sleepiness, as well.
A more plausible reason is that sleep disturbances or lack of sleep promotes the formation of amyloid plaques, through an unknown mechanism, and also, obviously, cause the patient to experience daytime sleepiness.
Both animal and human studies have shown a linkage between poor or restricted nighttime sleep and increased beta-amyloid protein deposits in the nervous system.
The results of the study suggest that the risk of AD could be reduced by appropriate intervention for individuals who have disturbed or insufficient sleep, whether this is  treating sleep disorders such as obstructive sleep apnea or insomnia, or modifying factors that act more broadly such as work-related sleep loss or poor sleep habits.
There is no cure yet for Alzheimer’s disease, so we have to do our best to prevent it… Prioritizing sleep may be one way to help prevent or perhaps slow this condition.”
Dr. Adam P. Spira, Ph.D., Lead Investigator
The study, Excessive Daytime Sleepiness and Napping in Cognitively Normal Adults: Associations with Subsequent Amyloid Deposition Measured by PiB PET was carried out by researchers from the National Institute on Aging (NIA), the Bloomberg School and Johns Hopkins Medicine and reported recently in the journal SLEEP.
Source:
This news article was written by News-Medical, based on a press release by Johns Hopkins School of Medicine and the research study itself.

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