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.

Monday, December 1, 2014

Imaging Shows Connection Breakdown in Early Alzheimer’s Brains

When is your doctor going to use this imaging modality to determine if your brain post-stroke has objective connection problems? And then create a stroke protocol to fix those problems? This is what you expect your doctor to be doing? Isn't it?
http://www.biosciencetechnology.com/news/2014/12/imaging-shows-connection-breakdown-early-alzheimer%E2%80%99s-brains?
Changes in brain connections visible on MRI could represent an imaging biomarker of Alzheimer's disease, according to a new study presented at the annual meeting of the Radiological Society of North America (RSNA).
 
Alzheimer's disease is the most common form of dementia. As many as 5 million Americans are affected, a number expected to grow to 14 million by 2050, according to the Centers for Disease Control and Prevention. Preventive treatments may be most effective before Alzheimer's disease is diagnosed, such as when a person is suffering from mild cognitive impairment (MCI), a decline in cognitive skills that is noticeable but not severe enough to affect independent function. Previous efforts at early detection have focused on beta amyloid, a protein found in abnormally high amounts in the brains of people with Alzheimer's disease.
 
For the new study, researchers looked at the brain's structural connectome, a map of white matter tracts that carry signals between different areas of the brain.
 
"The structural connectome provides us with a way to characterize and measure these connections and how they change through disease or age," said study co-author Jeffrey Prescott, radiology resident at Duke University Medical Center in Durham, N.C.
 
Prescott and colleagues analyzed results from 102 patients enrolled in a national study called the Alzheimer's Disease Neuroimaging Initiative (ADNI) 2. The patients had undergone diffusion tensor imaging (DTI), an MRI method that assesses the integrity of white matter tracts in the brain by measuring how easy it is for water to move along them.
 
"It is known that water prefers moving along the defined physical connections between regions in the brain, which makes DTI a great tool for evaluating the structural connectome," Prescott said.
 
The researchers correlated changes in the structural connectome with results from florbetapir positron emission tomography (PET) imaging, a technique that measures the amount of beta amyloid plaque in the brain. Increased florbetapir uptake corresponds with greater amounts of the protein.
 
The results showed a strong association between florbetapir uptake and decreases in strength of the structural connectome in each of the five areas of the brain studied.
 
"This study ties together two of the major changes in the Alzheimer's brain— structural tissue changes and pathological amyloid plaque deposition— and suggests a promising role for DTI as a possible diagnostic adjunct," Prescott said.
 
Based on these findings, DTI may offer a role in assessing brain damage in early Alzheimer's disease and monitoring the effect of new therapies.
 
"Traditionally, Alzheimer's disease is believed to exert its effects on thinking via damage to the brain's gray matter, where most of the nerve cells are concentrated," said Jeffrey Petrella, professor of radiology at Duke and senior author on the study. "This study suggests that amyloid deposition in the gray matter affects the associated white matter connections, which are essential for conducting messages across the billions of nerve cells in the brain, allowing for all aspects of mental function."
 
"We suspect that as amyloid plaque load in the gray matter increases, the brain's white matter starts to break down or malfunction and lose its ability to move water and neurochemicals efficiently," added Prescott.
 
The researchers plan to continue studying this cohort of patients over time to gain a better understanding of how the disease evolves in individual patients. They also intend to incorporate functional imaging into their research to learn about how the relationship between function and structure is affected with increasing amyloid burden.

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