Vascular endothelial growth factor in amyotrophic lateral sclerosis and other neurodegenerative diseases

  title={Vascular endothelial growth factor in amyotrophic lateral sclerosis and other neurodegenerative diseases},
  author={Elke Bogaert and Philip van Damme and Ludo Van Den Bosch and Wim Robberecht},
  journal={Muscle \& Nerve},
The angiogenic activity of vascular endothelial growth factor (VEGF) is well known. Recently, it has become evident that VEGF is involved in central nervous system physiology and may play a role in the pathogenesis of neurological diseases. In particular, it may be involved in the mechanism of motor neuron degeneration in amyotrophic lateral sclerosis (ALS), and has been hypothesized to be implicated in the pathogenesis of peripheral neuropathies such as occur in the so‐called POEMS syndrome… 

Roles of Vascular Endothelial Growth Factor in Amyotrophic Lateral Sclerosis

VEGF-B, presenting a single safety profile, protects motor neurons from degeneration in ALS animal models and, therefore, it will be particularly interesting to test its effects in ALS patients.

Vascular Endothelial Growth Factor Attenuates Neurodegenerative Changes in the NSC-34 Motor Neuron Cell Line Induced by Cerebrospinal Fluid of Sporadic Amyotrophic Lateral Sclerosis Patients

It is confirmed that VEGF exerts a neuroprotective effect on the NSC-34 cell line by attenuating the degenerative changes induced by ALS-CSF, and thus has therapeutic potential in sporadic ALS.


Neuroprotective Effect of Vascular Endothelial Growth Factor on Motoneurons of the Oculomotor System

Differences in VEGF availability that could contribute to the higher resistance of extraocular motoneurons to injury and neurodegenerative diseases are summarized.

Cellular and molecular mechanisms involved in the neuroprotective effects of VEGF on motoneurons

VEGF protects motoneurons from excitotoxic death and increases survival in animal models of ALS, and the potential use of VEGF as a therapeutic tool in ALS is counteracted by its vascular effects and by its short effective time frame.

Hypoxia‐inducible factors as neuroprotective agent in Alzheimer's disease

Keeping the HIF‐1α level by inhibiting the prolyl 4‐hydroxylase was effective to attenuate the nerve damage during hypoxia and postpone the incidence of AD.

Amyotrophic lateral sclerosis: all roads lead to Rome

It is postulated that other neuron‐specific defects, as those triggered by dynactin dysfunction, may account for a primary motor neuron disease that would represent ‘pure’ neuronal forms of ALS.



Expression of Vascular Endothelial Growth Factor and Its Receptors in the Central Nervous System in Amyotrophic Lateral Sclerosis

The similar expression patterns of VEGF and VEGFR2 suggests autocrine/paracrine effects on spinal motor neurons, and the reduction in their expression seen in ALS cases would support the hypothesis that reduced V EGF signaling may play a role in the pathogenesis of ALS.

Unraveling the mechanisms involved in motor neuron degeneration in ALS.

Along with errors in the handling of synaptic glutamate and the potential excitotoxic response this provokes, model systems highlight the involvement of nonneuronal cells in disease progression and provide new therapeutic strategies.

VEGF is increased in serum but not in spinal cord from patients with amyotrophic lateral sclerosis

The findings indicate that the capacity to synthesize VEGF is preserved even in the late stages of ALS, which might be consistent with a transient hypoxic component during the course of ALS but not with a persistant spinal hypoxia in theLate stages of the disorder.


A 3-fold increased risk of ALS is found among individuals homozygous for the AAG or AGG haplotypes, consistent with the findings of the previous study.