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.

Tuesday, July 23, 2019

Cumulative Cognitive Reserve Tied to Dementia Risk

I would like to know where this cognitive reserve test is and take it since I'm sure I lost all my previous cognitive reserve just surviving my stroke. So my cumulative reserve is only from the last 13 years.  How many more social and intellectual activities do I need to cram into a week? And when will I sleep? How much wine is needed?

Cumulative Cognitive Reserve Tied to Dementia Risk

Even with high Alzheimer's pathology, clinical dementia risk is affected

  • by Senior Staff Writer, MedPage Today
LOS ANGELES -- Higher scores on a measure of cumulative lifetime cognitive reserve reduced dementia risk even in the presence of brain pathologies, researchers reported here.
Older adults with the highest levels of lifespan cognitive reserve had a 39% lower risk of dementia than those with the lowest levels -- and dementia risk was less for these people even if they had Alzheimer's or vascular pathology, reported Xiuying Qi, PhD, and Weili Xu, MD, PhD, of Tianjin Medical University in China, and colleagues at the Alzheimer's Association International Conference (AAIC). The study was published simultaneously in JAMA Neurology.
Cognitive reserve has been proposed as a compensatory mechanism to explain why some people maintain better cognitive function with age-related brain changes or disease-related pathologies, noted co-author Hui Wu, also of Tianjin Medical University.
In much research, "one reserve-enhancing factor during a certain time period alone -- such as education, social, or cognitive activities -- has been considered as a proxy measure of cognitive reserve," Wu told MedPage Today. "However, emerging evidence has suggested that cognitive reserve is an active construct which develops from continued life experiences."
"Our findings suggest that accumulative educational and mentally-stimulating activities enhancing cognitive reserve might be a feasible strategy to prevent dementia, even in people with high Alzheimer's disease or vascular pathologies," she added.
To create a cumulative cognitive reserve measurement that spanned a lifetime, the researchers collected data about mental and social activities from 1,602 participants in the Rush University Memory and Aging Project, an ongoing community-based prospective cohort study. The average age of participants was nearly 80 and most participants (75.9%) were women.
The researchers constructed a lifespan cognitive reserve score that incorporated education, cognitive activities in early, mid-, and late life, social activity in late life, and social networks late in life. Participant scores were divided into tertiles -- lowest, middle, and highest.
Participants were dementia-free at baseline and were followed annually from 1997 to 2018 for a mean of 6 years. Over the follow-up period, 747 participants died and 611 underwent autopsy.
During follow-up, 386 participants developed dementia (24.1%), including 357 participants with Alzheimer's disease dementia (22.3%). Compared with people in the lowest tertile of lifespan cognitive reserve scores, people in the middle tertile had an adjusted HR of dementia of 0.77 (95% CI 0.59-0.99), and people in the highest tertile had an HR of 0.61 (95% CI 0.47-0.81).
Cognitive reserve was not associated with most brain pathologies on autopsy, and links between cognitive reserve and dementia remained significant after adjusting for brain pathologies (HR 0.60, 95% CI 0.42-0.86). The highest tertile of lifespan cognitive reserve scores had lower dementia risk even in the presence of high Alzheimer's disease pathology (HR 0.57, 95% CI 0.37-0.87) and any gross infarcts (HR 0.34, 95% CI 0.18-0.62).
"Lifespan cognitive reserve is a derived entity," noted Yonas Geda, MD, of the Mayo Clinic in Scottsdale, Arizona, who was not involved with the study. "Whenever you create a new construct by relying on other constructs, it can increase the risk of measurement error," he told MedPage Today.
But overall, "their finding makes sense and confirms what Mayo Clinic and others have reported -- that mentally stimulating activities decrease the risk of mild cognitive or dementia, possibly via the mechanism of cognitive reserve," Geda observed.
The study has several limitations: participants were volunteers and findings may not apply to other populations. Lifespan cognitive reserve factors were assessed by retrospective self-report, and unmeasured confounders also may have influenced results. And because brain changes occur many years before clinical diagnosis of dementia, reverse causality may be a factor.
The study was supported by grants from the National Institutes of Health, the Swedish Research Council, the National Natural Science Foundation of China, Demensfonden, the Konung Gustaf V:s och Drottning Victorias Frimurare Foundation, and the Alzheimerfonden. This project is part of CoSTREAM and received funding from the European Union's Horizon 2020 Research and Innovation Programme.
The authors disclosed no relevant relationships with industry.

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