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.

Thursday, January 28, 2016

Growth Factor in Brain Tied to Slower Mental Decline

How is your doctor testing and making sure your BDNF is adequate?
http://dgnews.docguide.com/growth-factor-brain-tied-slower-mental-decline?
Older people with higher amounts of brain-derived neurotrophic factor (BDNF) also had slower decline in their memory and thinking abilities than people with lower amounts of the protein, according to a study published in the January 27, 2016, online edition of the journal Neurology.
“This relationship was strongest among the people with the most signs of Alzheimer’s disease pathology in their brains,” said Aron S. Buchman, MD, Rush University Medical Center, Chicago, Illinois. “This suggests that a higher level of protein from BDNF gene expression may provide a buffer, or reserve, for the brain and protect it against the effects of the plaques and tangles that form in the brain as a part of Alzheimer’s disease.”
For the study, 535 people with an average age of 81 years were followed until death, for an average of 6 years. They took yearly tests of their thinking and memory skills, and after death, a neurologist reviewed their records and determined whether they had dementia, mild cognitive impairment (MCI) or no thinking and memory problems.
Autopsies were conducted on their brains after death, and the amount of protein from BDNF gene expression in the brain was then measured. The participants were part of the Rush Memory and Aging Project and the Religious Orders Study.
The rate of cognitive decline was about 50% slower for those in the highest 10% of protein from BDNF gene expression compared with the lowest 10%. The effect of plaques and tangles in the brain on cognitive decline was reduced for people with high levels of BDNF. In the people with the highest amount of Alzheimer’s disease hallmarks in their brains, cognitive decline was about 40% slower for people with the highest amount of protein from BDNF gene expression compared with those with the lowest amount.
On average, thinking and memory skills declined by about 0.10 units per year on the tests. Higher levels of protein from BDNF gene expression reduced the effect of plaques and tangles in the brain on cognitive decline by 0.02 units per year.
The researchers found that the plaques and tangles in the brain accounted for 27% of the variation in cognitive decline, demographics accounted for 3%, and BDNF accounted for 2%.
“More research is needed to confirm these findings, determine how this relationship between protein produced by BDNF gene expression and cognitive decline works and see if any strategies can be used to increase BDNF in the brain to protect or slow the rate of cognitive decline,” said Dr. Buchman.
He noted that the study does not prove that BDNF is the cause of a slower rate of cognitive decline; further work is needed to determine if activities which increase brain BDNF gene expression levels protect or slow the rate of cognitive decline in old age.
In an accompanying editorial, Michal Schnaider Beeri, PhD, Icahn School of Medicine at Mount Sinai, New York, New York, noted that exercise has been shown to increase levels of BDNF in the blood, but that the relationship between BDNF protein levels in the blood and in the brain is not clear.
SOURCE: American Academy of Neurology

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