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.

Sunday, October 29, 2017

Brain Structure Makes Some Resilient to Alzheimer’s - dendrite spines

You'll have to DEMAND your doctor provide you protocols that will create new dendritic spines.  And after s/he does that ask for proof that the protocols are working. You have to DEMAND accountability and responsibility from your doctors.  If you need to train your doctor; 16 posts on dendritic spines here,  1 post on dendritic spine formation, 25 posts on dendritic branching , 10 posts on dendrites.
. You need this for stroke recovery already, so if your doctor is ANY GOOD AT ALL they will already have stroke protocols for this. NO EXCUSES, the answers are out there at least for competent doctors to find.
http://neurosciencenews.com/alzheimers-brain-structure-7804/



Summary: According to researchers, the size, shape and number of dendritic spines in the brain may determine whether a person develops Alzheimer’s disease.
Source: University of Alabama at Birmingham.
The size, shape and number of dendritic spines in the brain may play a major role in whether someone gets Alzheimer’s disease, according to new research from the University of Alabama at Birmingham. Dendritic spines are sub-units of neurons that act as the connector to other neurons.
In findings published Oct. 24 in the Annals of Neurology, the research team showed, for the first time, that the presence of healthy dendritic spines conveyed a protective effect against Alzheimer’s in people whose brains had proteins associated with the disease.
“One of the precursors of Alzheimer’s is the development in the brain of proteins called amyloid and tau, which we refer to as the pathology of Alzheimer’s,” said Jeremy Herskowitz, Ph.D., assistant professor in the Department of Neurology, School of Medicine and lead author of the study. “However, about 30 percent of the aging population have amyloid and tau buildup but never develop dementia. Our study showed that these individuals had larger, more numerous dendritic spines than those with dementia, indicating that spine health plays a major role in the onset of disease.”
Neurons are constantly sending out long, thin dendritic spines in search of other neurons. When they connect, a synapse, or exchange of information between neurons, occurs. This is the basis for memory and learning.
“One obvious culprit in Alzheimer’s disease is the loss of dendritic spines and thus the loss of synapses,” said Herskowitz, who is the Patsy W. and Charles A. Collat Scholar in Neuroscience. “This would impair the ability to think, so the assumption has been that those without dementia had healthy spines and those with dementia did not. But no one had gone in to see if that was true.”
Herskowitz’s team studied brain samples from patients at memory clinics at Emory University. The control group did not have the Alzheimer’s pathology of amyloid plaques and tau tangles and never developed dementia. A second group had the Alzheimer’s pathology and progressed to the disease. The third group had the pathology, but no disease.
The researchers took thousands of microscopy images of the subject brains. Those images were then turned into 3-D images using novel, exclusive software. This allowed the team to look more fully at the shape and dimensions of each image.
“We first noted that the control group had more dendritic spines than the group with Alzheimer’s, which matched beautifully with existing historical data,” Herskowitz said. “But we also saw that the group with Alzheimer’s pathology but no disease also had more spines than the Alzheimer’s group. In fact, they had roughly the same spine density as the control group. What is even more exciting is that the ‘pathology but no disease’ group had very long spines, longer than both the control group and the disease group.”
Image shows neurons.
Neurons are constantly sending out long, thin dendritic spines in search of other neurons. When they connect, a synapse, or exchange of information between neurons, occurs. This is the basis for memory and learning. NeuroscienceNews.com image is credited to Alzheimer’s disease group.
Herskowitz says the longer spines demonstrated great plasticity, or ability to move. This indicates that they could navigate around or through amyloid plaques or tau tangles in their efforts to connect with other neurons.
“This provides an explanation of why some people are cognitively resilient to Alzheimer’s disease, even if they possess the typical Alzheimer’s pathology,” he said.
Herskowitz says that the high plasticity and density of dendritic spines in this population could be genetic. Another theory suggests that it could be the result of healthy lifestyle behaviors, such as good diet and exercise, which are known to be protective against dementia. It may be that the reason these behaviors are protective is that they help maintain spine health, plasticity and density.
The findings also offer a new target for slowing or preventing Alzheimer’s in the first place, Herskowitz says.
“This provides a target for drugs that would be designed to support and maintain dendritic spine health in an effort to rebuild neurons or prevent their loss,” he said. “This data suggests that rebuilding neurons is possible. And as we are better able to identify the increase of amyloid and tau early in the progression of the disease, even before symptoms arise, we might be able to one day offer a medication that can contribute to maintaining healthy dendritic spines in those with the Alzheimer’s pathology.”
About this neuroscience research article
Funding: Herskowitz credits the innovative 3-D imaging system used in the study to groundbreaking work done by UAB science and technology honors student Benjamin Boros. Funding for the study was provided by the National Institute on Aging, part of the National Institutes of Health, and the Alzheimer’s Association.
Source: Bob Shepard – University of Alabama at Birmingham
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is credited to Alzheimer’s disease group.
Original Research: Abstract for “Dendritic spines provide cognitive resilience against Alzheimer’s disease” by Benjamin D. Boros, Kelsey M. Greathouse BS, Erik G. Gentry BS, Kendall A. Curtis, Elizabeth L. Birchall BS, Marla Gearing PhD, and Jeremy H. Herskowitz PhD in Annals of Neurology. Published online October 22 2017 doi:10.1002/ana.25049

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