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Alzheimer's and Parkinson's May Feed Off Each Other

Diseases may join proteins to make each ailment worse, says study

MONDAY, Oct. 1, 2001 (HealthDayNews) -- Alzheimer's disease destroys memory and Parkinson's disease attacks the body's ability to move. But new research suggests these brain diseases are far from strangers to each other: A renegade protein in Alzheimer's patients may inspire another protein to cause Parkinson's.

Scientists in California don't know if the reverse -- Parkinson's contributing to Alzheimer's -- happens also. But they hope their research may mean that defusing one of these proteins, or both, may have a wider effect than narrowly targeting one disease.

"There is some sort of relationship between these two diseases beyond just coincidence," said study co-author Dr. Eliezer Masliah, a professor of neurosciences and pathology at the University of California at San Diego. "There might be similar mechanisms triggering these diseases. It might be possible that understanding one disease will help us understand the other." Up to one-third of Alzheimer's patients also get Parkinson's; some Parkinson's patients also have signs of Alzheimer's.

Researchers tinkered with the genes of mice so the animals produced one or both of two human proteins, known as human amyloid precursor protein (hAPP) and human alpha-synuclein (hSYN). The proteins, which occur naturally, can clump together and cause clogging in the brain and when they do, the result may be Alzheimer's and Parkinson's disease.

The findings appear in a recent issue of the Proceedings of the National Academy of Sciences.

The mice that were engineered to make only one of the proteins got only the disease linked to it. Mice that produced both proteins had worse cases of Alzheimer's and developed Parkinson's symptoms sooner than did the mice with only one protein linked to the diseases. Both proteins appear to contribute to disease by sticking to each other and causing clogs --- similar to those in a water pipe --- that block communication within the brain, Masliah said. "It's almost like a fatal interaction between these proteins," he said. "They interact with each other and change their physical structure in such a way that they become more prone to aggregate and form large sticky clumps."

The proteins also trigger a mechanism inside brain cells that tells them to commit suicide. When enough brain cells die, memory, movement and other functions are damaged.

Although similar causes may lie behind Parkinson's and Alzheimer's, they are far from identical diseases. "People with Alzheimer's often have cognitive problems early on, but they can easily move and walk about," said study co-author Dr. Lennart Mucke, a professor of neurology and neuroscience at the University of California, San Francisco. "Parkinson's causes problems with motor skills and movements, but [patients] are typically quite intact as far as memory is concerned."

An estimated 4 million Americans, including former President Ronald Reagan, suffer from Alzheimer's disease. Parkinson's disease affects 1 million people, including former Attorney General Janet Reno.

Dr. James Grisolia, a neurologist at Scripps Mercy Hospital in San Diego, cautioned that scientists still have much to learn about the causes of the two diseases, especially Parkinson's. "We don't have as clear a sense of what's going on in Parkinson's, what the underlying problem is and how it affects people," he said. It's not even clear if the clogged pathways are a cause, he added.

Scientists are especially limited because they can only look at the inner brain workings of animals, not living humans, he said.

The new research is promising but preliminary, he said. "After they've done further experiments, they may learn things that are very useful for people," Grisolia said. "It's certainly a very early step."

What To Do

Learn the facts about Alzheimer's disease from the Alzheimer's Association. And here's where you can take a look at a beta-amyloid protein.

Learn about Parkinson's disease from The American Parkinson Disease Association.

SOURCES: Interviews with Eliezer Masliah, M.D., professor of neurosciences and pathology, University of California at San Diego; Lennart Mucke, M.D., professor of neurology and neuroscience, UC San Francisco; James Grisolia, M.D., neurologist, Scripps Mercy Hospital, San Diego; Sept. 25, 2001, Proceedings of the National Academy of Sciences
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