| First Author | Ulatowski L | Year | 2014 |
| Journal | Neuroscience | Volume | 260 |
| Pages | 120-9 | PubMed ID | 24342566 |
| Mgi Jnum | J:208020 | Mgi Id | MGI:5560434 |
| Doi | 10.1016/j.neuroscience.2013.12.001 | Citation | Ulatowski L, et al. (2014) Vitamin E is essential for Purkinje neuron integrity. Neuroscience 260:120-9 |
| abstractText | alpha-Tocopherol (vitamin E) is an essential dietary antioxidant with important neuroprotective functions. alpha-Tocopherol deficiency manifests primarily in neurological pathologies, notably cerebellar dysfunctions such as spinocerebellar ataxia. To study the roles of alpha-tocopherol in the cerebellum, we used the alpha-tocopherol transfer protein for the murine version (Ttpa(-/)(-)) mice which lack the alpha-tocopherol transfer protein (TTP) and are a faithful model of vitamin E deficiency and oxidative stress. When fed vitamin E-deficient diet, Ttpa(-/)(-) mice had un-detectable levels of alpha-tocopherol in plasma and several brain regions. Dietary supplementation with alpha-tocopherol normalized plasma levels of the vitamin, but only modestly increased its levels in the cerebellum and prefrontal cortex, indicating a critical function of brain TTP. Vitamin E deficiency caused an increase in cerebellar oxidative stress evidenced by increased protein nitrosylation, which was prevented by dietary supplementation with the vitamin. Concomitantly, vitamin E deficiency precipitated cellular atrophy and diminished dendritic branching of Purkinje neurons, the predominant output regulator of the cerebellar cortex. The anatomic decline induced by vitamin E deficiency was paralleled by behavioral deficits in motor coordination and cognitive functions that were normalized upon vitamin E supplementation. These observations underscore the essential role of vitamin E and TTP in maintaining CNS function, and support the notion that alpha-tocopherol supplementation may comprise an effective intervention in oxidative stress-related neurological disorders. |
