Abstract:
:Haploinsufficiency of the SLC2A1 gene and paucity of its translated product, the glucose transporter-1 (Glut1) protein, disrupt brain function and cause the neurodevelopmental disorder, Glut1 deficiency syndrome (Glut1 DS). There is little to suggest how reduced Glut1 causes cognitive dysfunction and no optimal treatment for Glut1 DS. We used model mice to demonstrate that low Glut1 protein arrests cerebral angiogenesis, resulting in a profound diminution of the brain microvasculature without compromising the blood-brain barrier. Studies to define the temporal requirements for Glut1 reveal that pre-symptomatic, AAV9-mediated repletion of the protein averts brain microvasculature defects and prevents disease, whereas augmenting the protein late, during adulthood, is devoid of benefit. Still, treatment following symptom onset can be effective; Glut1 repletion in early-symptomatic mutants that have experienced sustained periods of low brain glucose nevertheless restores the cerebral microvasculature and ameliorates disease. Timely Glut1 repletion may thus constitute an effective treatment for Glut1 DS.
journal_name
Nat Communjournal_title
Nature communicationsauthors
Tang M,Gao G,Rueda CB,Yu H,Thibodeaux DN,Awano T,Engelstad KM,Sanchez-Quintero MJ,Yang H,Li F,Li H,Su Q,Shetler KE,Jones L,Seo R,McConathy J,Hillman EM,Noebels JL,De Vivo DC,Monani URdoi
10.1038/ncomms14152subject
Has Abstractpub_date
2017-01-20 00:00:00pages
14152issn
2041-1723pii
ncomms14152journal_volume
8pub_type
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