NEW YORK (Reuters Health) - Two naturally occurring proteins in the brain may combine to wreak havoc on normal brain function and contribute to Parkinson's disease onset, according to a report in the June issue of the journal Nature Medicine.

The conclusions are based on studies involving cultures of human brain nerve cells.

Parkinson's disease is marked by the loss of brain cells that produce the chemical dopamine, leading to symptoms such as tremor, rigidity and stiffness, slowed movement, and problems with balance and coordination. The exact cause is unknown, but many researchers believe that a combination of environmental factors, genetics and aging are at work.

The new study points to specific molecules that may cause the dopamine-producing neurons to die in the brains of patients with Parkinson's disease, explained lead investigator Dr. Bruce A. Yankner of The Children's Hospital in Boston, Massachusetts, during an interview with Reuters Health.

"It suggests that two proteins--alpha-synuclein and another protein called 14-3-3--may come together in a lethal combination, which could contribute to the development of Parkinson's disease," he said.

The researchers found that a protein complex containing the two substances could trigger a cell suicide mechanism in dopamine-producing nerve cells, but actually protected other types of nerve cells.

Until now, the combination of alpha-synuclein with 14-3-3 protein was not previously known to cause nerve cell degeneration, Yankner noted.

While the normal function of alpha-synuclein in the brain is unknown, the findings suggest that it may act to protect the brain, Yankner pointed out. "However, for unclear reasons, this protective function may be subverted to a detrimental toxic function in Parkinson's disease," he said.

"It is too early to make any clear predictions regarding treatment," Yankner said. "However, if the findings of this paper prove to be important for Parkinson's disease, then preventing alpha-synuclein from getting together with the 14-3-3 protein could be a new therapeutic approach to the disease."

SOURCE: Nature Medicine 2002;8:600-606.

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