Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 29,701 posts. Searching is done in the search box in upper left corner. I blog on anything to do with stroke. DO NOT DO ANYTHING SUGGESTED HERE AS I AM NOT MEDICALLY TRAINED, YOUR DOCTOR IS, LISTEN TO THEM. BUT I BET THEY DON'T KNOW HOW TO GET YOU 100% RECOVERED. I DON'T EITHER BUT HAVE PLENTY OF QUESTIONS FOR YOUR DOCTOR TO ANSWER.
Changing stroke rehab and research worldwide now.Time is Brain!trillions and trillions of neuronsthatDIEeach day because there areNOeffective 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.
Saturday, November 17, 2018
Researchers map how Alzheimer’s pathology spreads across brain networks
You are likely going to need a solution to this. So what the fuck followup is being
done by your doctor and stroke hospital? Or are they twiddling their
thumbs again waiting for SOMEONE ELSE TO SOLVE THE PROBLEM? ?
Capitalizing on recent advances in neuroimaging and genetic
biomarker research, scientists have been able to identify specific
pathways by which tau and beta-amyloid, two proteins that are hallmarks
of Alzheimer’s disease, accumulate in the brain over time. The
NIA-supported researchers also found that the patterns of tau and
beta-amyloid accumulation were related to specific genetic profiles,
providing better understanding of Alzheimer’s disease risk and possible
new avenues for diagnosis and monitoring of the disease.
Improved technology makes possible for intensive, side-by-side
comparisons of how tau and beta-amyloid spread in the brain in
distinctive patterns. Using this technology, researchers were able to
reveal nuances into how, even in disease, the brain follows a dynamic
and complex network of circuits and connections. The results were
reported in the Oct. 29 issue of Nature Medicine.
The study was led by Dr. Jorge Sepulcre and Dr. Keith Johnson of The
Gordon Center for Medical Imaging at Massachusetts General Hospital and
Harvard Medical School, and Dr. Reisa Sperling, director of the Center
for Alzheimer Research and Treatment at the Brigham and Women's Hospital
and professor of Neurology at Harvard Medical School. The team used
data from the Harvard Aging Brain Study and the Allen Human Brain Atlas. Patterns of pathology progression in the human brain using network-based PET imaging. (Image courtesy of Dr. Jorge Sepulcre.)In
a brain with Alzheimer’s disease, abnormal deposits of tau and
beta-amyloid do not randomly appear, but instead show unique spatial
patterns that follow the brain’s existing connected neural networks. To
better understand how tau and beta-amyloid interact with and influence
each other, the researchers looked closely at 3-D brain network and gene
maps and found that both tau and beta-amyloid were associated with
genes devoted to lipid metabolism, and that the APOE E4 gene – a risk
factor for Alzheimer’s disease – played a central role in the
relationships of these genetic networks.
The scientists found common genetic background for the malfunction of
both proteins. The findings showed that in addition to APOE, other
variations in genetic pathways shared by tau and beta-amyloid could
trigger their accumulation. The study also found that tau propagation
was associated with an axon-related (parts of neurons that pass messages
away from the cell body) genetic profile, while beta-amyloid’s spread
was connected with a dendrite-related (parts of neurons that receive
messages from other cells) genetic profile.
The researchers hope this new understanding of tau and beta-amyloid’s
propagation patterns can be combined with a person’s genetic profile to
help develop precision medicine approaches for improved diagnosis,
monitoring and therapies for Alzheimer’s disease in the brain. This research was funded in part by NIH grants K23EB019023, T32EB013180, R01HL137230, R01-AG027435-S1, P50-AG00513421, R01AG046396, P01-AG036694 and 1RF1AG052653-01A1. Reference: Sepulcre J et al. Neurogenetic contributions to amyloid beta and tau spreading in the human cortex. Nature Medicine. 2018 Oct 29 doi: 10.1038/s41591-018-0206-4. [Epub ahead of print]
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