Abstract
BackgroundVascular endothelial growth factor-A (VEGF-A) and chemokne ligand-2 (CCL2) levels have been examined in Amyotrophic Lateral Sclerosis (ALS) patients in Western countries. We measured these values in North Indian ALS patients, since these patients display considerably enhanced survival duration.MethodsSporadic ALS patients were included on the basis of El Escorial criteria. VEGF-A and CCL2 levels were analyzed in serum and cerebrospinal fluid (CSF) of 50 ALS patients using enzyme linked immunosorbent assay (ELISA) and compared with normal controls. Their levels were adjusted for possible confounders like cigarette smoking, alcohol and meat consumption.ResultsContrary to previous studies, VEGF-A was found to be elevated significantly in serum and CSF in ALS patient population studied. We also found an increase in CCL2 levels in CSF of these ALS patients. Serum and CSF from definite ALS revealed higher VEGF-A as compared to probable and possible ALS. CCL2 was unaltered between definite, probable and possible ALS. Univariate and multivariate analysis revealed a lack of association of smoking, alcohol and meat consumption with VEGF-A and CCL2 levels.ConclusionsVEGF-A upregulation may indicate an activation of compensatory responses in ALS which may reflect or in fact account for increased survival of North Indian ALS patients after disease onset. The intrathecal synthesis of CCL2 suggests the involvement of adult neural stem cells and microglial activation in ALS pathogenesis which needs further investigation.
Highlights
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder with genetic and clinical heterogeneity
Existing evidence suggests that Vascular endothelial growth factor-A (VEGF-A) delivery delays the onset and progression of Amyotrophic Lateral Sclerosis (ALS) in superoxide dismutase-1 (SOD1) mutated transgenic mouse model by activating phosphatidylinositol 3kinases (PI3-K)/ Akt anti apoptotic pathway [1,2]
Median cerebrospinal fluid (CSF) vascular endothelial growth factor (VEGF)-A concentration was significantly higher in ALS patients than controls (Figure 1B; p = 0.0001)
Summary
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder with genetic and clinical heterogeneity. Existing evidence suggests that Vascular endothelial growth factor-A (VEGF-A) delivery delays the onset and progression of ALS in superoxide dismutase-1 (SOD1) mutated transgenic mouse model by activating PI3-K/ Akt anti apoptotic pathway [1,2]. VEGF-A shown to be involved in proliferation and differentiation of adult mouse neural progenitor’s cells [3]. Vascular endothelial growth factor-A (VEGF-A) and chemokne ligand-2 (CCL2) levels have been examined in Amyotrophic Lateral Sclerosis (ALS) patients in Western countries. We measured these values in North Indian ALS patients, since these patients display considerably enhanced survival duration
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