Protein May Help Explain
How Parkinson's Arises
Excerpt By Amy Norton, Reuters Health

NEW YORK (Reuters Health) - Researchers may have found the missing link between two proteins involved in Parkinson's disease, a finding they say lends new insight into what goes wrong in the brain as the disease develops.

Mutations in the genes for the two proteins--called parkin and alpha-synuclein--are linked to separate, rare forms of inherited Parkinson's. But both parkin and alpha-synuclein are found in protein deposits called Lewy bodies that build up in the brains of all Parkinson's patients.

Studying how these two proteins may interact in the brain could lead to new ways to treat all forms of Parkinson's, the new study's lead author, Dr. Ted M. Dawson, told Reuters Health.

In experiments with cells, Dawson and his colleagues at Johns Hopkins University in Baltimore, Maryland, found that a third protein, called synphilin, acts as a go-between for parkin and alpha-synuclein. Parkin appears to interact with synphilin and use this protein to interact with alpha-synuclein, according to findings published in the October issue of Nature Medicine.

Parkinson's disease is a progressive neurological disorder marked by tremors, muscle rigidity, and balance and coordination problems. The destruction of brain cells that produce the chemical dopamine underlies these symptoms. These diseased cells are also marked by Lewy bodies. But no one knows why the cells die or whether the Lewy bodies help kill them.

These latest findings, according to the researchers, suggest that parkin plays an important role in regulating proteins associated with Lewy bodies in the brain, including alpha-synuclein and synphilin. Normally, parkin uses yet another protein, called ubiquitin, to ``tag'' other proteins for destruction. But if something goes wrong in the relationship among these proteins, this could lay the groundwork for the cell death seen in Parkinson's.

``We suspect that the destruction pathway and the action of ubiquitin might be very important in Parkinson's disease, that perhaps the altered destruction of alpha-synuclein could be the common thread in causing these (brain cells) to die,'' Dawson explained in a statement.

Problems with alpha-synuclein, Dawson told Reuters Health, now seem to be at the core of both the inherited and common forms of Parkinson's--even the rare form in which parkin is mutated, since parkin interacts with alpha-synuclein.

``This suggests we should focus our research attention on how to deal with abnormal alpha-synuclein,'' he said.

SOURCE: Nature Medicine 2001;7:1144-1150.

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