Vitamin E is essential for Purkinje neuron integrity
Open accessAbstract
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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Some studies observed that giving vitamin E lowers oxidative damage in the brain in vivo.
“Although vitamin E administration has been observed to decrease oxidative damage levels in brain in vivo in some studies82”
From Oxidative stress, dysfunctional glucose metabolism and Alzheimer disease (2019) · cites this paper as [82]
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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.
- Venue
- Neuroscience
- Publisher
- Elsevier BV
- Published
- 2014-02
- Volume
- 260
- Pages
- 120-129
- ISSN
- 0306-4522 (ISSN-L)
- 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 · 2013: 1 · 2012: 1
- FWCI
- 6.96
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- 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 › 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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