Editorial Board Members’ Collection Series: “Molecular Research on Neuroprotection”
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".
Deadline for manuscript submissions: 20 September 2024 | Viewed by 270
Special Issue Editors
Interests: neuronal protection; transgenic synRas mice; Ras and neuronal regeneration; Leucin-rich repeat kinase2 (LRRK2); functionalized nanoparticles; Nurr1; Parkinson
Special Issues, Collections and Topics in MDPI journals
2. Department of Systems Medicine, University of Rome Tor Vergata, 00133 Rome, Italy
3. Department of Human Sciences and Quality of Life Promotion, San Raffaele Roma Open University, 00166 Rome, Italy
Interests: neuroprotection; vascular diseases; aging; genetics; epidemiology; metabolic disorders; antioxidants; nutrition in vascular diseases
Special Issues, Collections and Topics in MDPI journals
Interests: spinal diseases (spinal cord injury, intervertebral disc degeneration, osteoporosis, etc.); pain; regeneration; stem cell; neuroprotection
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
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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Keywords
- neuronal connectivity
- neurotrophic factor signalling
- liquid–liquid phase separation (LLPS)
- Ras/MAPK signaling
- rasopathy
- protein phosphatase 2A
- Bax/Bad
- NFκB Signal-cascade
- ubiquitin system
- mitochondrial homeostasis
- protein quality control
- Alzheimer
- taupathy
- Parkinson
- Nurr1
- synuclein
