Gene and protein signatures in sporadic Parkinson's disease and a novel genetic model of PD.
High-throughput gene-based platform studies in human post-mortem substantia nigra from sporadic Parkinson's disease (PD) cases have revealed significant dysregulation of genes involved in biological processes linked to previously established neurodegenerative mechanisms both in sporadic and hereditary PD. These include protein aggregation, mitochondrial dysfunction, oxidative stress, cell cycle, vesicle trafficking, synaptic transmission, dopamine metabolism and cell adhesion/cytoskeleton maintenance. These observations have extended our current view on the molecular pathways underlying the etio-pathology of the disease and provided a basis for the development of a novel genetic model of sporadic PD, centered on gradual silencing/over-expression of the candidate genes. The uncovered signatures may serve as future predictive biomarkers for early PD diagnosis, disease progression and drug development.
Mandel
Silvia A
SA
Eve Topf Center for Neurodegenerative Diseases Research and Department of Pharmacology, Faculty of Medicine, Technion, Haifa, Israel. mandel@tx.technion.ac.il
Fishman
Tali
T
Youdim
Moussa B H
MB
D000818:Animals; D004195:Disease Models, Animal; D005786:Gene Expression Regulation; D020022:Genetic Predisposition to Disease / Q000235:genetics; D006801:Humans; D010300:Parkinson Disease / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D011506:Proteins / Q000235:genetics / Q000378:metabolism
D011506:Proteins