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Title: The C2578A, G1154A and G634C polymorphisms of the vascular endothelial growth factor gene as a risk factor for sporadic amyotrophic lateral sclerosis


Amyotrophic lateral sclerosis (ALS) is a fatal, progressive neurodegenerative disorder. Several disease pathomechanisms are proposed, including deficiency of trophic factors. In 2001, the relationship between VEGF and the risk of ALS was detected in a mouse model. The connection of the three -2578C/A, -1154G/A and -634G/C polymorphisms of the VEGF gene with the risk of ALS was documented in the population of Belgium, Sweden as well as the population of Birmingham. The aim of the presented study was to assess of the significance of the three polymorphic variants -2578C/A, -1154G/A and -634G/C of the VEGF gene as well as plasma VEGF levels with the risk of sporadic ALS. Genetic analysis included 271 cases with ALS and 464 healthy controls. Polymorphisms of the VEGF gene were analysed by the real time PCR or the PCR and restrictive enzymes digestion. Plasma VEGF levels was analysed in 60 patients with ALS and in 75 healthy controls. It was detected by ELISA. The presented study showed no relationship between the three functional polymorphisms of the VEGF gene and the risk of ALS; it showed no significance of the individual alleles, genotypes or haplotypes with risk of the disease. The study showed the higher frequency of the genotype with the A allele (AA and CA) of the -2578C/A polymorphism of the VEGF gene in female ALS cases as compared with male ALS cases. It also showed that the pair of the CGC and AAG haplotypes of the examined polymorphisms of the VEGF gene decreased the risk of ALS. The presented study did not show the differences between plasma VEGF levels in ALS cases with the controls.

Level of degree:

2 - studia doktoranckie

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Degree grantor:

Wydział Lekarski


Agnieszka Słowik

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tylko w bibliotece

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Biblioteka Medyczna Uniwersytetu Jagiellońskiego - Collegium Medicum

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Last modified:

Oct 7, 2019

In our library since:

Nov 21, 2012

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Edition name Date
ZB-112119 Oct 7, 2019




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