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Editorial Board Members’ Collection Series: “Molecular Research on Neuroprotection”
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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 April 2025 | Viewed by 4083

Special Issue Editors

Prof. Dr. Rolf Heumann

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Guest Editor
Department of Biochemistry II—Molecular Neurobiochemistry, Faculty of Chemistry and Biochemistry, Ruhr-Universität Bochum, 44801 Bochum, Germany
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
Dr. David Della-Morte

E-Mail Website
Guest Editor
1. Department of Neurology, Miller School of Medicine, University of Miami, Miami, FL 33136, USA
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
Prof. Dr. Inbo Han

E-Mail Website
Guest Editor
Department of Neurosurgery, CHA University School of Medicine, CHA Bundang Medical Center, Seongnam-si 13496, Republic of Korea
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

Manuscript Submission Information

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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

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Published Papers (2 papers)

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15 pages, 1930 KiB  
Review
NF-κB in Alzheimer’s Disease: Friend or Foe? Opposite Functions in Neurons and Glial Cells
by Barbara Kaltschmidt, Nele Johanne Czaniera, Wiebke Schulten and Christian Kaltschmidt
Int. J. Mol. Sci. 2024, 25(21), 11353; https://doi.org/10.3390/ijms252111353 - 22 Oct 2024
Viewed by 1189
Abstract
Alzheimer’s disease (AD) is a devasting neurodegenerative disease afflicting mainly glutamatergic neurons together with a massive neuroinflammation mediated by the transcription factor NF-κB. A 65%-plus increase in Alzheimer’s patients by 2050 might be a major threat to society. Hallmarks of AD are neurofibrillary [...] Read more.
Alzheimer’s disease (AD) is a devasting neurodegenerative disease afflicting mainly glutamatergic neurons together with a massive neuroinflammation mediated by the transcription factor NF-κB. A 65%-plus increase in Alzheimer’s patients by 2050 might be a major threat to society. Hallmarks of AD are neurofibrillary tangles (NFTs) composed of hyperphosphorylated tau and amyloid beta (Aβ) plaques. Here, we review the potential involvement of transcription factor NF-κB by hereditary mutations of the tumor necrosis factor pathway in AD patients. One of the greatest genetic risk factors is APOE4. Recently, it was shown that the APOE4 allele functions as a null allele in human astrocytes not repressing NF-κB anymore. Moreover, NF-κB seems to be involved in the repair of DNA double-strand breaks during healthy learning and memory, a function blunted in AD. NF-κB could be a friend to healthy neurons by repressing apoptosis and necroptosis. But a loss of neuronal NF-κB and activation of glial NF-κB in AD makes it a foe of neuronal survival. Hopeful therapies include TNFR2 receptor bodies relieving the activation of glial NF-κB by TNFα. Full article
(This article belongs to the Special Issue Editorial Board Members’ Collection Series: “Molecular Research on Neuroprotection”)
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18 pages, 1332 KiB  
Review
Innovative Strategies in 3D Bioprinting for Spinal Cord Injury Repair
by Daniel Youngsuk Kim, Yanting Liu, Gyubin Kim, Seong Bae An and Inbo Han
Int. J. Mol. Sci. 2024, 25(17), 9592; https://doi.org/10.3390/ijms25179592 - 4 Sep 2024
Cited by 2 | Viewed by 2228
Abstract
Spinal cord injury (SCI) is a catastrophic condition that disrupts neurons within the spinal cord, leading to severe motor and sensory deficits. While current treatments can alleviate pain, they do not promote neural regeneration or functional recovery. Three-dimensional (3D) bioprinting offers promising solutions [...] Read more.
Spinal cord injury (SCI) is a catastrophic condition that disrupts neurons within the spinal cord, leading to severe motor and sensory deficits. While current treatments can alleviate pain, they do not promote neural regeneration or functional recovery. Three-dimensional (3D) bioprinting offers promising solutions for SCI repair by enabling the creation of complex neural tissue constructs. This review provides a comprehensive overview of 3D bioprinting techniques, bioinks, and stem cell applications in SCI repair. Additionally, it highlights recent advancements in 3D bioprinted scaffolds, including the integration of conductive materials, the incorporation of bioactive molecules like neurotrophic factors, drugs, and exosomes, and the design of innovative structures such as multi-channel and axial scaffolds. These innovative strategies in 3D bioprinting can offer a comprehensive approach to optimizing the spinal cord microenvironment, advancing SCI repair. This review highlights a comprehensive understanding of the current state of 3D bioprinting in SCI repair, offering insights into future directions in the field of regenerative medicine. Full article
(This article belongs to the Special Issue Editorial Board Members’ Collection Series: “Molecular Research on Neuroprotection”)
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