Showing posts with label vitamin E. Show all posts
Showing posts with label vitamin E. Show all posts

Link between vitamin E, exposure to air pollution -- ScienceDaily

A new study from King's College London and the University of Nottingham
has found an association between the amount of vitamin E in the body,
exposure to particulate pollution and lung function. The paper adds to
growing evidence from previous studies suggesting that some vitamins may
play a role in helping to protect the lungs from air pollution.
Although the new study did not specifically demonstrate a protective
effect, it is the first to show a clear link between vitamin E
concentrations in the blood and exposure to fine particulate pollution
in the general population.

Vitamin E may delay decline in mild-to-moderate Alzheimer’s disease

Difficulty with activities of daily living often affect Alzheimer's patients, which is estimated to affect as many as 5.1 million Americans. These issues are among the most taxing burdens of the disease for caregivers, which total about 5.4 million family members and friends. New research from the faculty of Icahn School of Medicine at Mount Sinai working with Veterans Administration Medical Centers suggests that alpha tocepherol, fat-soluble Vitamin E and antioxidant, may slow functional decline (problems with daily activities such as shopping, preparing meals, planning, and traveling) in patients with mild-to-moderate Alzheimer's disease and decrease caregiver burden. There was no added benefit for memory and cognitive testing with the vitamin.

Vitamin E is essential for Purkinje neuron integrity.

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 α-tocopherol in the cerebellum, we used the Ttpa-/- mice which lack the 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 α-tocopherol in plasma and several brain regions. Dietary supplementation with α-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 α-tocopherol supplementation may comprise an effective intervention in oxidative stress-related neurological disorders.