Cellular and molecular mechanisms of VEGF at the level of the neuromuscular junction: implications for the treatment of ALS.

Neurodegenerative disorders (Alzheimer, Parkinson and Amytrophic lateral sclerosis (ALS)) form a group of diseases in which a selected cell population progressively dies, resulting in functional loss. Patients, suffering from any neurodegenerative disorder, have physical, mental and social disabilities and often die at young age since there is no pro-regenerative effective therapy available. Therefore, for all of these disorders, development of new therapies is absolutely required. However, before efficient therapies can emerge, we will first need to extend todays knowledge of underlying action mechanisms. The aim of this study is to unravel the cellular mechanisms by which the vascular endothelial growth factor (VEGF) acts on peripheral neurons and skeletal muscles, two tissues highly affected in ALS. To achieve this goal, we will use the major transgenic model for ALS (SOD1G93A mice), to determine to what extend muscle derived VEGF signaling can influence ALS disease progression and which mechanisms and cellular targets mediate this effect.

Keywords:VEGF, Alzheimer, Parkinson, ALS

Disciplines:Laboratory medicine, Palliative care and end-of-life care, Regenerative medicine, Other basic sciences, Other health sciences, Nursing, Other paramedical sciences, Other translational sciences, Other medical and health sciences