Autor(es): Felts Paul A,Smith Kenneth J,Gregson Norman A,Hughes Richard A C

Resumo: Long-term disability in Guillain-Barré syndrome (GBS) is associated with axonal, and some neuronal, degeneration. Brain-derived neurotrophic factor (BDNF) can prevent neuronal death following damage to motor axons and we have therefore examined the ability of BDNF to ameliorate the effects of experimental autoimmune neuritis (EAN), a model of GBS. Treatment of Lewis rats with BDNF (10 mg/kg/day) did not significantly affect the neurological deficit, nor significantly improve survival, motor function or motor innervation. The weight of the urinary bladder was significantly increased in control animals with EAN, but remained similar to normal in animals treated with BDNF. With the exception of a possibly protective effect indicated by bladder weight, this study suggests that BDNF may not provide an effective therapy for GBS, at least in the acute phase of the disease.

Imprenta: Journal of Neuroimmunology, v. 124, n. 1-2, p. 62-69, 2002

Identificador do objeto digital: 10.1016/S0165-5728(02)00017-6

Descritores: Guillain-Barre Syndrome - Biosynthesis ; Guillain-Barre Syndrome - Biochemistry ; Guillain-Barre Syndrome - Cell ; Guillain-Barre Syndrome - Cytopathology ; Guillain-Barre Syndrome - Pathogenesis ; Guillain-Barre Syndrome - Proteins ; Guillain-Barre Syndrome - Antibodies ; Guillain-Barre Syndrome - Clinical examination ; Guillain-Barre Syndrome - Immunology

Data de publicação: 2002

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