Editorial Board Members’ Collection Series: “Molecular Research on Neuroprotection”

Dear Colleagues,

We have developed a synRas animal mouse model that selectively expresses permanently activated Val12 Ras in neurons. This has allowed us to show that neuronal Ras activity is not only involved in brain plasticity but also in lesion-induced protection from neuronal cell death, as shown in motor neurons of the facial nucleus, in dopaminergic neurons of the substantia nigra, or after excitotoxic treatments in cortical neurons. We are now analysing variants of the voltage dependent anion channel (VDAC1) as possible mediators of the neuronal protection. Furthermore, leucine-rich repeat kinase 2 (LRRK2), containing a Ras-like homology domain (ROC), interacts with protein phosphatase 2A, thereby protecting cortical neurons from the toxic effects of parkinsonian LRRK2 mutants. We also show that not only the Ras /MAPK pathway but also the nuclear factor B (NFκB) signalling cascade is essential for the survival and regeneration of adult hippocampal neurons. As an initial step towards protein therapy, we have generated fusion proteins to carry the non-toxic domain of a bacterial import signal to deliver orphan transcription factor Nurr1 into the cell cytoplasm and the nucleus. We will demonstrate that the Nurr1 fusion protein has a protective effect against the neurotoxic 6-OHDA-induced cell death of dopamine-producing nerve cells.

Prof. Dr. Rolf Heumann
Dr. David Della-Morte
Prof. Dr. Inbo Han
Guest Editors

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