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Low levels of the vascular endothelial growth factor in CSF from early ALS patients

From the Department of Neurology (Drs. Devos, Moreau, De Seze, Brunaud-Danel, and Destée), R. Salengro Hospital, Department of Pneumology (Drs. Perez and Just), A. Calmette Hospital, and U 416 INSERM (Drs. Lassalle, Tonnel, and Just), Pasteur Institute of Lille, Multidisciplinary Center of ALS, Lille University Medical Centre, France.

Address correspondence and reprint requests to Dr. D. Devos, Hôpital R. Salengro, Clinique Neurologique, CHRU, F-59037 Lille cedex, France; e-mail: d-devos{at}chru-lille.fr

Deletion of the hypoxia-response element in the vascular endothelial growth factor (VEGF) promoter causes motor neuron degeneration in a mouse model. "At-risk" haplotypes with low circulating VEGF levels have been demonstrated in humans. Here the authors report low VEGF levels in the CSF of ALS patients during their first year of the disease, independently of VEGF promoter polymorphism. This finding early in ALS patients suggests a possible role for VEGF gene regulation in the pathogenesis of ALS.

Received November 12, 2003. Accepted in final form January 31, 2004.

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