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.
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial Share Alike License (http://creativecommons.org/licenses/by-nc-sa/3.0), which permits unrestricted non-commercial use, distribution and reproduction in any medium provided that the original work is properly cited and all further distributions of the work or adaptation are subject to the same Creative Commons License terms.
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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