2011
DOI: 10.1016/j.neulet.2011.03.088
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Vascular endothelial growth factor-B is neuroprotective in an in vivo rat model of Parkinson's disease

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Cited by 52 publications
(36 citation statements)
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“…VEGF-B treatment reduced stroke volume in a middle cerebral artery ligation model and increased survival of retinal ganglion cells in an optic nerve crush injury model (7), and VEGF-B knockout mice suffered severe strokes and exacerbated retinal ganglion cell death in both injury models (7)(8)(9). VEGF-B has also been used with promising results in Parkinson's disease (10) and amyotrophic lateral sclerosis models (11).…”
mentioning
confidence: 99%
“…VEGF-B treatment reduced stroke volume in a middle cerebral artery ligation model and increased survival of retinal ganglion cells in an optic nerve crush injury model (7), and VEGF-B knockout mice suffered severe strokes and exacerbated retinal ganglion cell death in both injury models (7)(8)(9). VEGF-B has also been used with promising results in Parkinson's disease (10) and amyotrophic lateral sclerosis models (11).…”
mentioning
confidence: 99%
“…In another study, VEGF-B 186 was used to test its neuroprotective effect in a PD model since it is more diffusable and hardly binds to extracellular matrix than VEGF-B 167 (Olofsson et al, 1996b;Poesen et al, 2008). In this study, a single dose of VEGF-B 186 (3µg/rat) rescued dopaminergic neurons from death in the caudal sub region of substantia nigra in rats (Falk et al, 2011). Thus, as a potent neuronal and vascular protective factor, VEGF-B may have therapeutic implications in PD treatment.…”
Section: Parkinson's Diseasementioning
confidence: 81%
“…Indeed, the up-regulated transcriptional activation of VEGF-B in response to midbrain neurodegenerative challenges was observed in Parkinson's Disease (PD), and VEGF-B produced by astrocytes and motor neurons exerted a neuroprotective affect. 22 , 100 Preclinical studies in PD 101 and amyotrophic lateral sclerosis model 22 had shown promising results, despite the lack of clinical studies. VEGF-B treatment rescued brain neurons from apoptosis in stroke mouse 21 and protected cultured primary motor neurons against degeneration, 22 with little retinal neovascularization effect.…”
Section: Introductionmentioning
confidence: 99%
“…The co-expression of VEGF-B with FAs oxidation relative mitochondrial genes was observed in rat midbrain, suggesting the mitochondria as the target site. 102 Moreover, VEGF-B possessed the considerably robust survival ability, 101 , 102 as a single VEGF-B 186 protein treatment at a dose of 3 mg per rat partially protected dopaminergic fibers in the striatum and rescued the dopaminergic neurons in the caudal sub-region of the substantianigra. 101 …”
Section: Introductionmentioning
confidence: 99%