Research Advances Are Being Made : Health: Efforts toward understanding Alzheimer’s ‘are going like gangbusters.’ Drugs that may slow the disease are being tested.
The prognosis for Alzheimer’s patients nowadays is still not good. Cognex, the one drug approved to treat the condition, only relieves symptoms.
But, according to Carl W. Cotman, a prominent psychobiologist who directs UC Irvine’s research into Alzheimer’s, efforts toward understanding the disease “are going like gangbusters. It’s an amazing rate of progress.” Drugs that may slow the disease are being tested.
Researchers have long known that the disease kills cells in the brain’s cortex, memory cells that don’t regenerate. The effect, which worsens over the years, is partially erased memories and an inability to store new ones. Cotman says the newest, most promising hypothesis is that Alzheimer’s is actually normal body processes running amok. Brain cells receive orders to destroy themselves and comply, but the orders are bogus.
Programmed cell death, or apoptosis, is an established fact in all body cells, Cotman says. Under certain circumstances, a cell will trigger its own program for self-destruction.
“It’s kind of like a society that would ask an undesirable person to go take a permanent walk into the wilderness. We think it initially was an adaptive mechanism that is used to take out bad-performing cells or sick cells, and it’s just running away in Alzheimer’s disease.”
A protein called beta amyloid is exuded by neurons for some unknown purpose and accumulates in the fluids outside the cell. Everyone has a small amount of it, but with age, the concentration builds. In some people the proteins spontaneously condense into a sticky, fibrous substance that cannot be dissolved.
Like plaque on teeth, this substance binds to the outside of the cells and somehow stimulates or simulates the signal for cell suicide. “It triggers a process intended to be triggered by something else,” Cotman says.
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So far, a few high-risk factors have been identified for Alzheimer’s. A head injury or cardiovascular disease seems to signal a greater likelihood of developing Alzheimer’s. Researchers are also on the track of genetic indicators and have a few promising clues.
Meanwhile, researchers are experimenting with ways of slowing the Alzheimer’s progress.
“We’re testing whether physical activity might produce something in the system that interferes with the Alzheimer’s process,” Cotman says. “It’s a shot in the dark, but we’re encouraged. We’re getting some indications, but it’s too early.
“It also turns out that education is an offset. Apparently if you stimulate the brain, it becomes more resistant. It’s ‘use it or lose it,’ exactly.”
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Vitamin C and E sometimes are prescribed to protect against, perhaps even slow, the progress of Alzheimer’s, but their effectiveness has not been proved. “There is solid evidence that the vitamins protect against heart and blood vessel problems due to aging, and they’re safe to take in moderate quantities, so why not?” Cotman says. “I take a gram of C and 800 units of E daily, but it varies person to person.”
Most diseases are studied through animal tests, but for Alzheimer’s “there’s no animal model; that’s the big problem,” Cotman says. “We haven’t figured out how to give rats Alzheimer’s yet. So you’re into cell culture and simpler models, and so whatever you’ve got, you’ve got to work on it until it’s safe, then put it in man to find out. That’s very time-consuming.”
Something similar to Alzheimer’s does occur in animals, Cotman says. Other primates show similar symptoms in old age. Old dogs sometimes suffer from memory problems, making it literally impossible to teach them new tricks.
“The real efforts in Alzheimer’s research are only a few years old,” Cotman says, “but we’re getting more and more solid leads all the time.”
