Ketogenic diet reverses behavioral abnormalities in an acute NMDA receptor hypofunction model of schizophrenia
Journal Publication ResearchOnline@JCUAbstract
[Extract] Recent transcriptomic, proteomic and metabolomics studies suggest that abnormal glucose and energy metabolism may underlie the pathophysiology of schizophrenia (Harris et al., 2013). We hypothesized that interventions that influence energy metabolism might be therapeutically beneficial. One such intervention is the high-fat/low-carbohydrate ketogenic diet (KD) that has been effectively used in drug-resistant epilepsies (Paoli et al., 2013). To test our hypothesis we fed mice with KD for 3 weeks and induced acute NMDA receptor hypofunction by MK-801 (dizocilpine) administration to model the hypo-glutamatergic state that has been hypothesized to contribute to schizophrenia (Amann et al., 2010). We measured psychomotor hyperactivity and stereotyped behavior, social withdrawal and working memory deficits, reflecting the positive, negative and cognitive symptoms of schizophrenia, respectively (Jones et al., 2011).
Journal
Schizophrenia Research
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Volume
169
ISBN/ISSN
1573-2509
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Pages Count
3
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Publisher
Elsevier
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Publisher Location
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Date
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EISSN
N/A
DOI
10.1016/j.schres.2015.10.041