Parkinson’s disease (PD) is a neurodegenerative disorder characterized by loss of dopaminergic (DA) neurons in the substantia nigra pars compacta (SNc) and the consequent depletion of striatal dopamine, resulting in both motor and non-motor impairment. Till now, PD can only be treated symptomatically. Failure to translate neuroprotective strategies from pre-clinical to clinical studies might result from the use of animal models in which cell death is caused by limited mechanisms of action. We aim at confirming the involvement of system xc- or the cystine/glutamate antiporter in PD pathology by using a dual-hit model combining peripheral inflammation and toxin-induced models i.e. proteasome inhibition.
|Status||Published - 2015|
|Evenement||Center for Neurosciences, PhD day - Brussels, Belgium|
Duur: 27 feb 2015 → …
|Seminar||Center for Neurosciences, PhD day|
|Periode||27/02/15 → …|