NGFN-PLUS
Biomarkers of the common Parkinson pathway: Autosomal recessive Parkinson shows α-Synuclein induction and synaptic pathology
| Coordinator: | Prof. Dr.Georg Auburger | |
| Institution: | Klinikum der Goethe-Universität Frankfurt, Zentrum für Neurologie und Neurochirurgie - Molekulare Neurogenetik | |
| Homepage: | www.kgu.de/znn/neurologie |
During the past financing period NGFN2, we worked on the identification of the PARK6 disease gene and tested the value of skin biopsies of PARK6 patients and of brain from PARK1 and PARK6 mouse mutants as models of Parkinson’s disease (PD).
Now in NGFNplus we want to identify those molecules, which make diagnostics possible to discover the PD-risk before clinical onset or to quantify disease progression versus therapy benefit after onset. As biomarkers of all cellular processes we will analyze the expression levels of detectable mRNAs and proteins.
Since experiments in Drosophila-flies demonstrated that PARK6 initiates the same pathological mechanisms as PARK2, we will now study also skin-fibroblasts from PARK2 patients and at-risk individuals, as well as the brain from PARK2 mouse mutants, to compare them with our previous PARK6 and PARK1 data.
With the same approach we hope to understand, which metabolic pathways of the body are altered particularly early in PD. So far our results suggest that the synaptic contacts between nerve cells are affected particularly early, and that their energy production, their signal transmission and their adhesion are impaired, while increased oxidative stress is damaging these structures. The insights gained about the mechanism of disease will open new avenues towards therapy.
One novel therapy will be texted already in patient fibroblasts: The reduction of oxidative stress. Our aim is to slow down the degenerative process or to stop it.
Further Coordinators:
Now in NGFNplus we want to identify those molecules, which make diagnostics possible to discover the PD-risk before clinical onset or to quantify disease progression versus therapy benefit after onset. As biomarkers of all cellular processes we will analyze the expression levels of detectable mRNAs and proteins.
Since experiments in Drosophila-flies demonstrated that PARK6 initiates the same pathological mechanisms as PARK2, we will now study also skin-fibroblasts from PARK2 patients and at-risk individuals, as well as the brain from PARK2 mouse mutants, to compare them with our previous PARK6 and PARK1 data.
With the same approach we hope to understand, which metabolic pathways of the body are altered particularly early in PD. So far our results suggest that the synaptic contacts between nerve cells are affected particularly early, and that their energy production, their signal transmission and their adhesion are impaired, while increased oxidative stress is damaging these structures. The insights gained about the mechanism of disease will open new avenues towards therapy.
One novel therapy will be texted already in patient fibroblasts: The reduction of oxidative stress. Our aim is to slow down the degenerative process or to stop it.
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