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 (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 Aβ accumulation and behavioral impairments in the Tg2576 mice.
| Original language | English |
|---|---|
| Pages (from-to) | 758-764 |
| Number of pages | 7 |
| Journal | Journal of Neurochemistry |
| Volume | 90 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - Aug 2004 |
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Keywords
- Alzheimer's disease
- Amyloidosis
- Head trauma
- Oxidative stress
- Vitamin E
ASJC Scopus subject areas
- Biochemistry
- Cellular and Molecular Neuroscience
Cite this
Vitamin E reduces amyloidosis and improves cognitive function in Tg2576 mice following repetitive concussive brain injury. / Conte, Valeria; Uryu, Kunihiro; Fujimoto, Scott; Yao, Yuemang; Rokach, Joshua; Longhi, Luca; Trojanowski, John Q.; Lee, Virginia M Y; McIntosh, Tracy K.; Praticò, Domenico.
In: Journal of Neurochemistry, Vol. 90, No. 3, 08.2004, p. 758-764.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Vitamin E reduces amyloidosis and improves cognitive function in Tg2576 mice following repetitive concussive brain injury
AU - Conte, Valeria
AU - Uryu, Kunihiro
AU - Fujimoto, Scott
AU - Yao, Yuemang
AU - Rokach, Joshua
AU - Longhi, Luca
AU - Trojanowski, John Q.
AU - Lee, Virginia M Y
AU - McIntosh, Tracy K.
AU - Praticò, Domenico
PY - 2004/8
Y1 - 2004/8
N2 - 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 Aβ accumulation and behavioral impairments in the Tg2576 mice.
AB - 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 Aβ accumulation and behavioral impairments in the Tg2576 mice.
KW - Alzheimer's disease
KW - Amyloidosis
KW - Head trauma
KW - Oxidative stress
KW - Vitamin E
UR - http://www.scopus.com/inward/record.url?scp=3342903288&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=3342903288&partnerID=8YFLogxK
U2 - 10.1111/j.1471-4159.2004.02560.x
DO - 10.1111/j.1471-4159.2004.02560.x
M3 - Article
C2 - 15255955
AN - SCOPUS:3342903288
VL - 90
SP - 758
EP - 764
JO - Journal of Neurochemistry
JF - Journal of Neurochemistry
SN - 0022-3042
IS - 3
ER -