Vitamin E reduces amyloidosis and improves cognitive function in Tg2576 mice
following repetitive concussive brain injury.

Conte V, Uryu K, Fujimoto S, Yao Y, Rokach J, Longhi L, Trojanowski JQ, Lee VM,
McIntosh TK, Pratico D.

Head Injury Center, University of Pennsylvania, Philadelphia, Pennsylvania,
USA.

Abstract 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 (Abeta) 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 behavi{*filter*}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 Abeta 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 Alphabeta accumulation
and behavi{*filter*}impairments in the Tg2576 mice.

PMID: 15255955 [PubMed - in process]

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