Media for Cognitive Retention Therapy Program

A simple and rapidly spreading therapy for Alzheimer's patients now has a national training base in Las Vegas.

And it is easy to see why the Canadian founders of Cognitive Retention Therapy decided this summer to establish a U.S. headquarters. They expect hundreds of elder-care providers to seek training in upcoming years, and Las Vegas will be a convenient destination, said John Asby, program director of the Calgary-based company.

In one year, 60 providers with 220 clients have started using the drug-free techniques, which promise to reverse memory loss associated with dementia.

Therapists merely talk with the patients, using written exercises and field trips that remind individuals about their lives. For example, one retired pilot was told to read paragraphs about pilot training or the Wright Brothers aloud, then to answer multiple-choice questions. He then progressed to visiting an aerospace museum.

"It's simplistic to look at it in its form, and the results are amazing," said Julie Buss, program director for CRT at Care4Life, a Las Vegas home health company that has signed on 10 CRT clients in four months. It was also her enthusiasm for the program that guided CRT officials to set up shop in Las Vegas.

No specific research on CRT has been conducted, though a study is in the works with the Arizona-based research center Sun Health, Ashby said.

But experience has shown the methods improve scores on the Mini Mental State Examination, a measure of cognitive mental status, by about four points, he said.

"Generally speaking, (the scores of Alzheimer's patients) don't go up at all, they just go down," Ashby said.

The science is based on the research of his mother, Dr. Mira Ashby, who was awarded Canada's highest civil honor for research on the learning process in people with brain injuries.

John Ashby and Sue Jaspar, executive director of the CRT program, two years ago began perfecting their system through trial and error.

The basic concept is that a brain stores memories in different parts. CRT uses the example of a lemon: The taste of a lemon is stored in one section, while the size and shape are stored in another.

"You do not actually lose information, you just cannot find it," Ashby said. "The pathway is lost, and you can't put the memory together. This reinforces new pathways. Your brain wants to be able to remember."

CRT gives therapists packets of exercises called modules. Most are generic — like ones on the 1920s, '30s or '40s — and are designed to apply to a large number of elderly clients.

Anecdotal results show individuals regain their self sufficiency and return to normal activities that were hindered by memory loss, like golfing or telling jokes at the dinner table.

"There's a reengagement with the family, and they do things they've stopped doing," Jaspar said. "They stand a lot taller, their confidence is improved, and they are participating in their own disease process."

The sessions are currently only available through private payment. Leaders hope that upcoming studies will help the therapy qualify for Medicare reimbursement and that other insurance companies may follow.

Care4Life charges $65 an hour and meets with clients twice per week, and it gives a $10-per-session discount to individuals who are using the agency's home health service, Buss said.

The 1 1/2-day training sessions will take place at Acacia Springs, the independent living facility where Care4Life's office is based. Geriatric care managers, psychologists and nurses who specialize in dementia care are expected to be interested in the training, Ashby said.

And as simple as the therapy sounds, he predicts that individuals will seek out professionals to administer it.

"These structured exercises are very, very difficult for the average person to do," he said. "If it was as simple as sitting down with Mom and Dad and having a jolly old conversation, I would assure you everybody would do that."

People who drink three or more servings of juice per week have a 76 percent lower risk of developing Alzheimer's than those who only drink juice less than once a week, according to a research study released Thursday.

The study, conducted by Dr. Qi Dai, assistant professor of medicine at the Vanderbilt University Medical Center and his colleagues – will be published in the September issue of the American Journal of Medicine.

The team collected information on how much fruit and vegetable juices from 1,836 dementia-free people over the age of 65 from the Seattle area. They measured their cognitive functions every two years for about a decade.

All of the participants were Japanese in origin because of the low rate of the disease among the Japanese population. However, Dai said Japanese people living incidence of Alzheimer's than those still living in Japan because of changes to lifestyle and diet.

Dai said researchers first thought that high intakes of antioxidant vitamins such as vitamins C, E and carotene might help protect against the disease, but he sought to study the role that another type of antioxidant, called polyphenols, play in reducing risk.

The study does not determine what kinds of juices, or in what conbinations, they benefit people the most. Dai said he and his colleagues want to study that next. The study would also look at the best way to prepare fruits and vegetables for optimal results. “If you’re peeling an apple the majority of polyphenol just goes away, but as a juice it’s rich in it,” he said.

Memory Lapses May Indeed be Alzheimer's
Lindsey Tanner – The Associated Press Chicago

A study found that a disturbing number of cases, embarrassing “senior moments” such as forgetting a recent conversation or drawing a blank on someone’s name may really be a sign of Alzheimer's after all.

Chicago scientists reached that conclusion after autopsies on the brains of 134 older people who had appeared to be mentally normal, apart from some subtle forgetfulness.

Occasional forgetfulness is often written off as a normal part of growing old and nothing to get alarmed about. And in most cases, that is probably true.

But the scientists found to their surprise that the brains of more than one third of the participants were riddled with waxy protein clumps and other signs of degeneration that are hallmarks of Alzheimer's disease.

The study “questions the acceptability of minor episodic memory loss in older adults as normal,” said Dr. Carol Lippa, director of the memory disorders program at Drexel University College of Medicine in Philadelphia. She had no part in the study.

The study appears in today’s issue of Neurology, the American Academy of Neurology’s scientific journal.

Dallas Anderson, an Alzheimer's scientist at the National Institute on Aging, which funded the research, called the results “very plausible and hopeful.”

Anderson noted that scientists are trying to pinpoint the earliest point in the Alzheimer's disease process.

Participants in the study had amounts of brain deterioration similar to those found in Alzheimer's patients who were severely debilitated by the mind-robbing disease before their deaths.

WASHINGTON (AP) -- Scientists have discovered molecular janitors that clear away a sticky gunk blamed for Alzheimer's disease -- until they get old and quit sweeping up.

The finding helps explain why Alzheimer's is a disease of aging. More importantly, it suggests a new weapon: drugs that give nature's cleanup crews a boost.

"It's a whole new way of thinking in the Alzheimer's field,'' said Dr. Andrew Dillin, a biologist at California's Salk Institute for Biological Studies who led the new research.

The discovery, published Thursday by the journal Science, was made in a tiny roundworm called C. elegans.

What do worms have to do with people? They're commonly used in age-related genetics research, and the new work involves a collection of genes that people harbor, too. Dillin's team from Salk and the neighboring Scripps Research Institute already is on the trail of potential drug candidates.

About 4.5 million Americans have Alzheimer's, a toll expected to more than triple by 2050 as the population grays. The creeping brain disease gradually robs sufferers of their memories and ability to care for themselves, eventually killing them. There is no known cure; today's drugs only temporarily alleviate symptoms.

Nor does anyone know what causes Alzheimer's. The lead suspect is a gooey protein called beta-amyloid. All brains contain it, although healthy cells somehow get rid of excess amounts. But beta-amyloid builds up in Alzheimer's patients, both inside their brain cells and forming clumps that coat the cells -- plaque that is the disease's hallmark.

Thursday's study reveals one way that cells fend off amyloid buildup, and that natural aging gradually erodes that detoxification process.

"Every pathway we can discover that modifies amyloid provides us with new drug targets,'' said Dr. Sam Gandy, a neuroscientist at Philadelphia's Thomas Jefferson University and an Alzheimer's Association spokesman. "This now opens up a new pathway'' for developing anti-Alzheimer's drugs.

Worms can't get Alzheimer's. So Dillin's team used roundworms that produce human beta-amyloid in the muscles of the body wall. As the worms age, amyloid builds up until it eventually paralyzes them; they can wiggle only their heads.

Then the researchers altered genes in a pathway called insulin/IGF-1, long known to be key in controlling lifespan. Making the worms live longer protected them from paralysis.

So in slowing down normal aging, something also slowed the buildup of toxic amyloid. But what?

One, named HSF-1, breaks apart amyloid and disposes of it, the researchers discovered. Natural aging slows HSF-1, so it can't keep up with the necessary detoxification.

Another protein called DAF-16 jumps in to help buy a little more time, by clumping extra amyloid together in a way that makes it less toxic.

That was a key finding, Dillin said: Until recently, scientists thought amyloid clumps, or plaques, were the bigger problem. His research supports more recent findings that smaller amyloid tendrils inside cells are the really poisonous form.

"We think probably the HSF-1 is the preferred way'' to dispose of amyloid, Dillin said. "By the time you see the plaques, it's too late.''

Mammals, including people, have these same proteins. Dillin now is repeating his experiment in mice to be sure they work the same way.

Scientists already are creating drugs to try to rid the brain of amyloid. These cleanup proteins point to a novel way to do that. The hope: Create drugs that boost their effects, and amyloid might not build up in the first place. Dillin said some initial drug attempts are showing promise in his worms.

The proteins won't be the brain's only natural amyloid scrubbers, noted Gandy, whose own research points toward involvement of another age-related gene.

"We all knew that aging increases the risk for Alzheimer's,'' but not why, Gandy explained. "Now there's a direct link. ... It gives the molecular connection between aging and Alzheimer's.''

And this process of "toxic aging'' likely plays a role in still other neurodegenerative diseases, Dillin said, citing similar research with Huntington's disease.

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