ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2015
Excessive α-tocopherol exacerbates microglial activation and brain injury caused by acute ischemic stroke.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
- Comparative neuroprotective and antioxidant roles of vitamin E isoforms: a review.Journal of clinical biochemistry and nutrition · 2026Review
- The Neuroprotective Effects of Alpha-Tocopherol as an Anti-Inflammatory Agent: Mechanistic Insights and Therapeutic Challenges.Nutrients · 2026Review
- Association between comprehensive dietary antioxidant index and stroke: mediating role of oxidative stress.Journal of clinical biochemistry and nutrition · 2026Article
- Role of CD36 in central nervous system diseases.Neural regeneration research · 2024Review
- Inflammation Biomarker Response to Oral 2-Hydroxybenzylamine (2-HOBA) Acetate in Healthy Humans.Inflammation · 2023Article
- Inducible miR-1224 silences cerebrovascular Serpine1 and restores blood flow to the stroke-affected site of the brain.Molecular therapy. Nucleic acids · 2023Article
- Biological Potential, Gastrointestinal Digestion, Absorption, and Bioavailability of Algae-Derived Compounds with Neuroprotective Activity: A Comprehensive Review.Marine drugs · 2022Review
- Enjoy Carefully: The Multifaceted Role of Vitamin E in Neuro-Nutrition.International journal of molecular sciences · 2021Review
- Brain tocopherol levels are associated with lower activated microglia density in elderly human cortex.Alzheimer's & dementia (New York, N. Y.) · 2020Article
- Essential Dietary Bioactive Lipids in Neuroinflammatory Diseases.Antioxidants & redox signaling · 2018Review
- Therapeutic potential of vitamin E and its derivatives in traumatic brain injury-associated dementia.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2018Review
- Phytoestrogen isoflavone intervention to engage the neuroprotective effect of glutamate oxaloacetate transaminase against stroke.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- Glutamate oxaloacetate transaminase enables anaplerotic refilling of TCA cycle intermediates in stroke-affected brain.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- α-Tocopherol at Nanomolar Concentration Protects Cortical Neurons against Oxidative Stress.International journal of molecular sciences · 2017Article
- Metabolic profiling reveals biochemical pathways and potential biomarkers associated with the pathogenesis of Krabbe disease.Journal of neuroscience research · 2016Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
The vitamin E family includes both tocopherols and tocotrienols, where α-tocopherol (αTOC) is the most bioavailable form. Clinical trials testing the therapeutic efficacy of high-dose αTOC against stroke have largely failed or reported negative outcomes when a "more is better" approach to supplementation (>400 IU/d) was used. This work addresses mechanisms by which supraphysiologic αTOC may contribute to stroke-induced brain injury. Ischemic stroke injury and the neuroinflammatory response were studied in tocopherol transfer protein-deficient mice maintained on a diet containing αTOC vitamin E at the equivalent human dose of 1680 IU/d. Ischemic stroke-induced brain injury was exacerbated in the presence of supraphysiologic brain αTOC levels. At 48 h after stroke, S100B and RAGE expression was increased in stroke-affected cortex of mice with elevated brain αTOC levels. Such increases were concomitant with aggravated microglial activation and neuroinflammatory signaling. A poststroke increase in markers of oxidative injury and neurodegeneration in the presence of elevated brain αTOC establish that at supraphysiologic levels, αTOC potentiates neuroinflammatory responses to acute ischemic stroke. Exacerbation of microglial activation by excessive αTOC likely depends on its unique cell signaling regulatory properties independent of antioxidant function. Against the background of clinical failure for high-dose αTOC, outcomes of this work identify risk for exacerbating stroke-induced brain injury as a result of supplementing diet with excessive levels of αTOC.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.