An article in the Albuquerque Journal reads:

Alzheimer's Study Making Progress
By, Daniel Haney; Tha Associated Press

Some doctors would enjoy nothing more that poking around inside your brain.

After giving it a thorough going-over, they would confidently predict whether in five or 10 or maybe even 20 years you will lose the whole works to Alzheimer's disease.

Not that you would want to know this necessarily, since nothing can be done yet to stop the disease.  Still doctors appear surprisingly close to getting their wish. 

Experimantal technology is opening a window on the living brain, catching the first clear look at the mess Alzheimer's makes as it happens.  It builds on the standard imaging machines, such as PET scanners, that are somethimes used on people with suspected Alzheimer's disease.  Those can reveal whether parts of the brain are shrunken.  But short of cutting open the skull, there has been no way to tease out the errant gummy proteins that distinguish Alzheimer's from normal gray matter.

Until now.  The new approach is also a PET scan, but unlike anything now available, it lights up these misplaced proteins

"It's an icreadile first step," says neil Buckholtz, dementia; chief at the National Institute on Aging.

Two competing teams in Pittsburgh and Los Angeles have produced these scans in the past year.  No one knows whether either approach will make it into routine use.  But many believe something like them eventully will

"They are both really magnificent examples of how far the technology has come," says William Thies, the Alzheimer's Association's medical director.  "Here we have the ability to actually image something the human brain that previously could only be seen in an autopsy"

Ordinary PET scans trace radioactive sugar as it moves through the brain, revealing how vigorously it is used in various parts.  While this offers clues to how well the brain functions, it says little specifically about Alzheimer's.

Tor that, doctors must examine slices of brain tissur under a microscope, looking for protein fragments called beta amyloid that lodge between brain cells and probably contribute to the death.

But revealing anyloid in a living brain is another matter since it
s invisible on an ordinary brain scan.  For years, researchers have puzzled over how they could introduce an amyloid-seeking chemical into someone's head so it would show up.

Seven years ago, Chester Mathis, a radio-chemist, and Dr. William Klunk, a psychiatrist, teamed up to find something that would.  Much tinkering later, the team created Pittsburgh Compound B, a radioactive dye ready to try on people.

That happened last winter at Upplala University in Sweden.  Doctors injected the dye into 14 volunteers.  Each had early stage Alzheimer's.  The rest were normal.  Each took a 90 minute turn inside the PET scanner.

The scans showed little accumulation in the healthy volunteers.  But the Alzheimer's patients were clearly different..  On the scans, the dyed amyloid shows up tomato red and yellow.  The colors ooze ominously across the frontal cortex and the temporal and parietal regions.

"Whan I saw it for the first time, I felt like, 'Wow, there it is,'" says Klunk.  "There is amyloid in the brain.  You're looking at it, after trying for so long."

At an Alzheimers conferaence in July in Stockholm, the Uppsala scans were shown in public for the first time.

"Several thousand people were in the auditorium, and they gaspped," remembers Mathis.  "It was exactly what pathologists see when they apply stains to human tissue.  Everybody realized it was in the right places."

The Pittsburgh team's main competition is a group at UCLA headed by Jorge Barrio, a pharamacologist, and Drol Gary Small, a psychiatrist.  They have developed a synthetic chemical called FDDNP and tagged it with radioactive flourine-18 so it will show up on PET scans.  Plaque is hydrophobic, meaning it resists water, and FDDNP is designed to home in on any hydrophobic tissue.

In testing on about 70 older people, their scans show buildups of hydrophobic matterial, presumably plaque, in areas of the brain where it is known to accumulate during Alzheimer's disease.

However, finding people with obvious Alzheimer's is unlikely to be the most important use of any such brain scan.  "This is driven by the idea that it will probably be easier to protect the brain before it's damaged than to repair damaged cells later, so let's find it as soon as possible," says Small.

If preliminary results hold up, the scans may reveal the first moments of Alzheimer's r even warn of accumulating amyloid years before the disease triggers its first vague symptoms.

But for now, nothing proven to reverse, stop or slow the progression of Alzheimer's disease.  Nevertheless, many doctors are confident they will eventually have medicines that arrest the buildup of amyloid during the period so it never causes problems.

Some common treatments are already being studied for this.  They include vitamin E, cholesterol pills, anti-inflammatory painkillers, estrogen, folate and ginkgo biloba.  Many more are being designed from scratch.  Thies estimates that pharmaceutical companies have already developed humdreds or maybe even thousands of compounds intended to manipulate amyloid in some way.

The problem is proving any of them work.  Alzheimer's symptoms vary from person to person.  Often the disease progresses slowly.  It could take several years of testing to prove that a drug has any effect on memory and reasoning.

"No CEO will commit to what will be a long, large exensive trial when there is no decent endpoint," says Dr. Samuel Gandy, director of the neurosciences institute at Thomas Jefferson University.

Offering such an endpoint could be the first big use of the new scans. Experts envision testing an amyloid drug on a dozen or two volunteers, then following them for a few months to see if it changes the amount of amyloid on their brain scans.  If it does, then developers would feel more confident taking the drug into large-scale testing to see if it slows symptoms, too.

In fact, the scans will allow the ultimate challenc\ge of the central dogma of Alzheimer's disease or whether it's simply a byproduct of it.  "The major question is, "And if you prevent it from forming, will that prevent the disease?"
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