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1.
J Neurochem ; 90(3): 758-64, 2004 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-15255955

RESUMEN

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 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 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 behavioral impairments in the Tg2576 mice.


Asunto(s)
Amiloidosis/prevención & control , Conmoción Encefálica/tratamiento farmacológico , Encéfalo/metabolismo , Trastornos del Conocimiento/prevención & control , Dinoprost/análogos & derivados , Vitamina E/farmacología , Amiloide/metabolismo , Péptidos beta-Amiloides/análisis , Péptidos beta-Amiloides/metabolismo , Amiloidosis/etiología , Animales , Antioxidantes/farmacología , Encéfalo/patología , Encéfalo/fisiopatología , Química Encefálica , Conmoción Encefálica/complicaciones , Conmoción Encefálica/fisiopatología , Trastornos del Conocimiento/etiología , Suplementos Dietéticos , Dinoprost/metabolismo , Modelos Animales de Enfermedad , Ensayo de Inmunoadsorción Enzimática , Femenino , Ratones , Ratones Transgénicos , Actividad Motora/efectos de los fármacos , Estrés Oxidativo/efectos de los fármacos , Fragmentos de Péptidos/análisis , Fragmentos de Péptidos/metabolismo , Vitamina E/metabolismo
2.
Curr Opin Crit Care ; 10(2): 105-9, 2004 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-15075719

RESUMEN

PURPOSE OF REVIEW: Currently, no neuroprotective therapies have been shown to reduce the secondary neuronal damage occurring after traumatic brain injury. Recent studies have addressed the potentiality of hyperoxia to ameliorate brain metabolism after traumatic brain injury. In this article, we present the principles of oxygen transport to the brain, the effects of hyperoxia on cerebral metabolism, and the role of lactate in brain metabolism after traumatic brain injury. RECENT FINDINGS: It has been shown that hyperoxia obtained by increasing the inspired fraction of oxygen results in a decreased cerebral lactate concentration measured in the extracellular space using the microdialysis. However, the brain oxygen delivery is not substantially improved by eubaric hyperoxia and the ratio between lactate and pyruvate (a better indicator of the cellular redox state than lactate alone) is not changed by hyperoxia. In addition, it has been shown the lactate might be an alternative fuel for neurons during the acute postinjury phase. SUMMARY: At present, there is no evidence supporting any clinical benefit of hyperoxia in brain-injured patients, and the meaning of posttraumatic brain extracellular lactate accumulation should be further investigated.


Asunto(s)
Lesiones Encefálicas/terapia , Oxígeno/administración & dosificación , Animales , Encéfalo/metabolismo , Lesiones Encefálicas/metabolismo , Humanos , Oxigenoterapia Hiperbárica , Italia , Ácido Láctico/metabolismo , Oxígeno/metabolismo
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