The establishment of a link between VEGF, hypoxia and ALS pathogenesis placed angiogenic factors and oxidative stress at the focal point for further studies. Recreation of a phenotype strikingly similar to that of mutant SOD1 mouse and human ALS, like muscle weakness and atrophy owing to lower motor neuron degeneration was observed following the targeted deletion of the hypoxia response element (HRE) from promoter of mouse vascular endothelial growth factor (VEGF). The crucial link between vasculature, angiogenic molecules and motor neuron degeneration has thus been constantly scrutinized. In this review, we have proposed to correlate human, in vitro and cadaveric studies so as to find out whether molecules like VEGF and various others, at the interface of neurovascular network and oxidative stress, have a prognostic, diagnostic and therapeutic potential for treatment of a fatal neurodegenerative disorder namely ALS.
Keywords: Amyotrophic Lateral Sclerosis (ALS), angiogenin, biomarkers, neurovascular, optineurin, oxidative stress, soluble VEGFR1 (sVEGFR1)/soluble fms-like tyrosine kinase-1 (sFLT-1), transactive response DNA-binding protein 43 (TDP-43), MND, (NCDs)