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Researchers Reveal a New Twist in Torsion Dystonia

Courtesy of Guy Caldwell CLEARING THE DRAIN: (Left) The worm expresses polyglutamine GFP in both the presence and absence of torsin. (Right) A Caenorhabditis elegans torsin protein, TOR-2 (red), localizes to sites of polyglutamine green fluorescent protein (GFP) aggregation (green) in a worm cell. A movement disorder can start as a twinge. A child's leg turns in while walking. Writing becomes difficult, painful. For many, these types of diseases--broadly termed dystonias--progress no fur

Brendan Maher
Courtesy of Guy Caldwell
 CLEARING THE DRAIN: (Left) The worm expresses polyglutamine GFP in both the presence and absence of torsin. (Right) A Caenorhabditis elegans torsin protein, TOR-2 (red), localizes to sites of polyglutamine green fluorescent protein (GFP) aggregation (green) in a worm cell.


A movement disorder can start as a twinge. A child's leg turns in while walking. Writing becomes difficult, painful. For many, these types of diseases--broadly termed dystonias--progress no further than persistent muscle cramps. Yet in many children affected by rare, heritable, early-onset dystonia, a generalized movement disorder called torsion dystonia develops as well. The disorder can affect the entire body: Opposing muscles work against each other, twisting the posture, causing repetitive movements, or contorting arms and legs into unnatural positions. Oftentimes, the earlier in life symptoms appear, the worse they get.

To uncover the roots of this dominant trait, which has only 30% to 40% penetrance,...

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