Despite lifelong restriction of dietary galactose, individuals with classic galactosemia suffer from various long-term complications, including speech, cognitive and movement problems. The underlying mechanisms are unknown, and treatments are limited. To shed light on this issue, Ryan et al. investigated long-term disease outcomes using a GALT-null Drosophila model of galactosemia that they developed previously. They report that, similar to patients, mutant flies develop a long-term movement defect that worsens rapidly with age. As little as 2.5% residual expression of the missing enzyme, GALT, is sufficient to improve long-term outcomes, whereas low-level exposure to galactose during development had no effect. These findings challenge current theories about long-term complications of galactosemia and confirm that this fly model will be useful for further studies of the disease. Page 796
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IN THIS ISSUE| 01 November 2012
Exploring long-term outcomes of galactosemia in flies
Online Issn: 1754-8411
Print Issn: 1754-8403
Written by editorial staff. © 2012. Published by The Company of Biologists Ltd.
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Dis Model Mech (2012) 5 (6): 707.
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Exploring long-term outcomes of galactosemia in flies. Dis Model Mech 1 November 2012; 5 (6): 707. doi:
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