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Alzheimer's Research Into Brain Injury And Damaging Protein Yields Surprising Results

Posted by Jane Akre
Friday, August 29, 2008 11:23 AM EST
Category: Major Medical, Protecting Your Family
Tags: Alzheimer's Disease, Alzheimer's and Dementia, Dementia, FDA and Prescription Drugs

People recovering from brain injury were actually observed to have more amyloid protein as they recovered, not less as researchers thought.



 IMAGE SOURCE: ©iStockphoto/ closeup render of neuron brain cell/ author: Henrik5000


In the rush to discover the underlying causes of Alzheimer’s disease, researchers have focused on the protein amyloid beta.

The protein is thought to play a key role in accelerating the creation of the sticky clumps of plaque that are a marker for the brain devastating disease.

The theory was that plaque was increased following a brain injury resulting from a car accident, an assault, or a fall and that led to a higher risk of Alzheimer’s disease.

Instead researchers found the opposite occurred.

Researchers at Washington University in St. Louis and the University of Milan studied 18 patients with a severe brain injury as they were coming out of a coma. For the first time, researchers measured, hour-by-hour the changes in the amount of amyloid beta.

The research teams placed a catheter in the brain of the recovering patient to capture fluid in the spaces between cells where the amyloid beta protein normally accumulates. They expected to see the amyloid beta levels to be high around the time of injury, then taper off.  

But surprisingly, they saw the protein levels increase as patients recovered. Patients who did not recover saw their amyloid beta protein levels fall.  The better a patient’s overall neurological status, the higher the protein levels rose.

The conclusion is that protein may be an indicator of how the brain cells are communicating across synapses.

“We can’t at this point rule out a very early spike in amyloid right after a brain injury. It raises a lot more questions than it answers,”  Dr. David Brody of Washington University said to Reuters in a telephone call.

The theory for therapy was that removing the plaque would slow progression of the disease, now that question is on hold.

"We haven't measured how brain injury affects amyloid beta inside cells, nor have we determined whether brain injury affects the ability of amyloid beta to form small aggregates that may be especially harmful," he explains. 

Dr. Brody admits that measuring the space between cells may have been insufficient to gauge the amyloid inside of cells and that this study is just the beginning.

Another theory is that injury may reduce the brain’s ability to offset Alzheimer’s related damage, making symptoms show up sooner.

The results are reported in Science. 

Scientists have already established that plaque clutters brains of people with dementia and Alzheimer’s and that tangles of protein may interrupt the brain’s functioning. In rat studies, rats injected with a form of beta-amyloid showed characteristics of Alzheimer’s.

But plaque has also been observed inside the brains of otherwise healthy people who do not have dementia.  It may remain that the type of beta-amyloid plaque is what’s crucial.

The race is on to make some inroad into Alzheimer's and its mind-robbing devastation before one in eight baby boomers, or about 10 million Americans, face its effects as predicted. 26 million people worldwide are affected and the numbers are rising dramatically according to the Alzheimer’s Association. 

Medicare spending will jump to $38 billion in 2025, when the boomers reach the age for nursing home admission. #

1 Comment

Posted by Amy
Monday, September 01, 2008 4:16 PM EST

This is great news since we will hopefully be able to prevent Alzheimer's in TBI survivors once we figure out how this works

Comments for this article are closed.

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