Cited by 122Antioxidant Activity and Oxidative StressNeurological Disease Mechanisms and TreatmentsGenetic Neurodegenerative Diseases

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Vitamin E is essential for Purkinje neuron integrity

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Ulatowski, L., Parker, R., Warrier, G., Sultana, R., Butterfield, D.A., Manor, D.·2014·Neuroscience

DOI 10.1016/j.neuroscience.2013.12.001PMC PMC3943241

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Abstract

α-Tocopherol (vitamin E) is an essential dietary antioxidant with important neuroprotective functions. α-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 α-tocopherol transfer protein for the murine version (Ttpa(-/)(-)) mice which lack the α-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.

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Authors: Ulatowski, L., Parker, R., Warrier, G., Sultana, R., Butterfield, D. A., & Manor, D.
Affiliations: Case Western Reserve University (US)
Cornell University (US)
University of Kentucky (US)
Corresponding author: Manor, D.
ORCID: Ulatowski, L.
Parker, R.
Warrier, G.
Butterfield, D.A.
Venue: Neuroscience
Publisher: Elsevier BV
Published: 2014-02
Volume: 260
Pages: 120-129
ISSN: 0306-4522 (ISSN-L)
DOI: 10.1016/j.neuroscience.2013.12.001
PMC: PMC3943241
OpenAlex: W1972998914
Cited by: 122
References: 87
Citations by year: 2026: 4 · 2025: 4 · 2024: 5 · 2023: 10 · 2022: 10 · 2021: 16 · 2020: 11 · 2019: 11 · 2018: 12 · 2017: 10 · 2016: 15 · 2015: 7 · 2014: 5
FWCI: 6.96
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Neuroscience (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: National Institutes of Health (2r01dk067494-07)
National Institute of Diabetes and Digestive and Kidney Diseases (DK 067494, R01-DK067494)
Topics: Health Sciences › Medicine › Biochemistry (medical) › Antioxidant Activity and Oxidative Stress
Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Genetic Neurodegenerative Diseases
Keywords: vitamin E, alpha-tocopherol, alpha-tocopherol transfer protein, vitamin E deficiency, cerebellum, Purkinje cells, oxidative stress, protein nitrosylation, dendritic branching, neuronal atrophy, spinocerebellar ataxia, motor coordination, cognitive impairment, dietary supplementation, neuroprotection
MeSH terms: Animals, Carrier Proteins, Cerebellum, Motor Activity, Purkinje Cells, Tyrosine, Vitamin E Deficiency, Prefrontal Cortex, Mice, Knockout, Oxidative Stress, alpha-Tocopherol, Mice

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Vitamin E is essential for Purkinje neuron integrity

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