Mitochondrial function as pharmacological target in Parkinson’s disease

Parkinson’s disease (PD) is neurodegenerative disorders including motor symptoms linked to the loss of dopaminergic neurons in the Substantia Nigra pars compacta. The etiology is still unknow, but data suggest an important role of mitochondrial dysfunction in the onset of this disease. The vulnerability of dopamine neurons seems to be related to their particularly high energy demand due to their very large number of axon terminals. Such morphological and physiological characteristics also cause high levels of mitochondrially-derived oxidative stress. This makes the mitochondria a critical target for potential disease-modifying therapy. The fpresent project aims to investigate whether the use of compounds that improve mitochondrial function while controlling oxidative stress can lead to a neuroprotective effect and increase the survival of vulnerable dopaminergic neurons. Demonstrating this effect could lead to the development of new drugs for the treatment of PD based on the restoration of mitochondrial efficiency.

Faculty Supervisor:

Louis-Eric Trudeau

Student:

Partner:

University of Foggia

Discipline:

Life Sciences

Sector:

Education

University:

Université de Montréal

Program: