Abstract
Parkinson's disease (PD) is a neurodegenerative motor disorder characterized by the loss of dopaminergic neurons. This loss of dopaminergic neurons is the pathological hallmark of the disease that results in the characteristic motor syndrome. Restoration of dopamine levels is the basis of current therapy; however, this does not tackle the cause of the disease. While the aetiology of PD remains mostly elusive, mitochondrial dysfunction has been linked to (at least) part of the PD cases. In this review we discuss recent findings in Drosophila melanogaster showing that stimulation of the electron transport chain is beneficial for PD fly models showing Complex I defects and discuss the possible clinical applications of these findings.
Publication types
-
Research Support, Non-U.S. Gov't
-
Review
MeSH terms
-
Animals
-
Disease Models, Animal
-
Dopamine / metabolism*
-
Dopaminergic Neurons / metabolism
-
Dopaminergic Neurons / pathology
-
Drosophila Proteins / genetics
-
Drosophila Proteins / metabolism*
-
Drosophila melanogaster
-
Electron Transport Complex I / metabolism*
-
Humans
-
Mitochondria / metabolism*
-
Mitochondria / pathology
-
Parkinson Disease / metabolism
-
Parkinson Disease / pathology
-
Parkinson Disease / therapy*
-
Protein Serine-Threonine Kinases / genetics
-
Protein Serine-Threonine Kinases / metabolism*
-
Ubiquitin-Protein Ligases / genetics
-
Ubiquitin-Protein Ligases / metabolism
Substances
-
Drosophila Proteins
-
Ubiquitin-Protein Ligases
-
PINK1 protein, Drosophila
-
Protein Serine-Threonine Kinases
-
park protein, Drosophila
-
Electron Transport Complex I
-
Dopamine