Vitamin E reduces amyloidosis and improves cognitive function in Tg2576 mice following repetitive concussive brain injury
Open accessAbstract
Traumatic brain injury is a well‐recognized environmental risk factor for developing Alzheimer's disease. Repetitive concussive brain injury (RCBI) exacerbates brain lipid peroxidation, accelerates amyloid (Aβ) formation and deposition, as well as cognitive impairments in Tg2576 mice. This study evaluated the effects of vitamin E on these four parameters in Tg2576 mice following RCBI. Eleven‐month‐old mice were randomized to receive either regular chow or chow‐supplemented with vitamin E for 4 weeks, and subjected to RCBI (two injuries, 24 h apart) using a modified controlled cortical impact model of closed head injury. The same dietary regimens were maintained up to 8 weeks post‐injury, when the animals were killed for biochemical and immunohistochemical analyses after behavioral evaluation. Vitamin E‐treated animals showed a significant increase in brain vitamin E levels and a significant decrease in brain lipid peroxidation levels. After RBCI, compared with the group on regular chow, animals receiving vitamin E did not show the increase in Aβ peptides, and had a significant attenuation of learning deficits. This study suggests that the exacerbation of brain oxidative stress following RCBI plays a mechanistic role in accelerating Αβ accumulation and behavioral impairments in the Tg2576 mice.
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Only two reports examining repetitive TBI in Tg2576 mice showed increased Aβ in addition to behavioral impairment at chronic post-injury time points.
“Only two reports examining repetitive TBI in Tg2576 mice showed increased Aβ in addition to behavioral impairment at chronic post-injury time points (165, 233).”
From The Inflammatory Continuum of Traumatic Brain Injury and Alzheimer’s Disease (2018) · cites this paper as [233]
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- Authors
- Conte, V., Uryu, K., Fujimoto, S., Yao, Y., Rokach, J., Longhi, L., Trojanowski, J. Q., Lee, V. M., McIntosh, T. K., & Praticò, D.
- Affiliations
- University of Pennsylvania (US)
- United States Department of Veterans Affairs (US)
- Florida Institute of Technology (US)
- ORCID
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 2004-07-05
- Volume
- 90
- Issue
- 3
- Pages
- 758-764
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- OpenAlex
- W2026311918
- Cited by
- 164
- References
- 9
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 7 · 2023: 2 · 2022: 16 · 2021: 9 · 2020: 3 · 2019: 8 · 2018: 6 · 2017: 8 · 2016: 9 · 2015: 9 · 2014: 13 · 2013: 11 · 2012: 11
- FWCI
- 4.73
- Type
- journal article
- Language
- en
- Open access
- green
- hdl.handle.net
- Licence
- Locations
- Journal of Neurochemistry (publishedVersion)
- PubMed (publishedVersion)
- Archivio Istituzionale della Ricerca (Universita Degli Studi Di Milano) (submittedVersion, other-oa)
- Funders
- National Institute on Aging (P01AG011542, AG 11542)
- National Heart, Lung, and Blood Institute (HL-69835, R01HL069835)
- National Institute of General Medical Sciences (R01GM034690, GM34690)
- National Institute of Neurological Disorders and Stroke (R01NS040978, NS 40978, NS-08803)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Epidemiology › Traumatic Brain Injury Research
- Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Keywords
- vitamin E, traumatic brain injury, Alzheimer's disease, amyloid-beta, amyloidosis, lipid peroxidation, oxidative stress, cognitive impairment, learning deficits, Tg2576 mice, controlled cortical impact, dietary supplementation
- MeSH terms
- Amyloid, Amyloidosis, Animals, Antioxidants, Brain, Brain Chemistry, Brain Concussion, Cognition Disorders, Disease Models, Animal, Enzyme-Linked Immunosorbent Assay, Female, Mice, Transgenic, Motor Activity, Peptide Fragments, Vitamin E, Dinoprost, Amyloid beta-Peptides, Oxidative Stress, Dietary Supplements, Mice
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