Novel Approaches to the Regeneration and Repair of the Nervous System: Neuronal Reprogramming

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: 31 May 2024 | Viewed by 997

Special Issue Editor

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Guest Editor
Medical College of Georgia, Augusta, GA 30912, USA
Interests: microRNAs; neuronal reprogramming; spinal cord injury; amyotrophic lateral sclerosis

Special Issue Information

Dear Colleagues,

While adult neurogenesis has been observed in specific brain regions, the potential for generating new neurons in the adult human central nervous system is severely constrained. Despite significant advances in medicine, the task of replenishing lost neurons following central nervous system injuries and neurodegenerative diseases remains highly challenging. A promising avenue to address this challenge is in situ neuronal reprogramming, an emerging approach that involves converting somatic cells into induced neurons capable of functioning like existing neurons. However, bridging the gap between fundamental scientific research and clinical applications in this field poses a substantial challenge. Neuronal reprogramming involves various obstacles, including cell death, low reprogramming efficiency, difficulties with off-target gene delivery, incomplete reprogramming, and the unintended generation of undesirable cell types. Effectively overcoming these critical hurdles is essential to pave the way for a future where neuronal reprogramming has transformed the landscape of medicine and human health. This Special Issue aims to gather original research articles and review papers specifically focused on neuronal reprogramming, both in vivo and in vitro, with a particular emphasis on addressing the aforementioned obstacles. By exploring innovative solutions to these challenges, we can envision a future where the potential of neuronal reprogramming is fully harnessed to revolutionize medical interventions and enhance overall human health.

Dr. Xuanyu Chen
Guest Editor

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  • neuronal reprogramming
  • astrocyte
  • NG2 cells
  • brain injury
  • spinal cord injury
  • AAV
  • gene delivery
  • neurodegenerative diseases

Published Papers (1 paper)

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14 pages, 3058 KiB  
Ectopic Expression of Neurod1 Is Sufficient for Functional Recovery following a Sensory–Motor Cortical Stroke
by Jessica M. Livingston, Tina T. Lee, Tom Enbar, Emerson Daniele, Clara M. Phillips, Alexandra Krassikova, K. W. Annie Bang, Ines Kortebi, Brennan W. Donville, Omadyor S. Ibragimov, Nadia Sachewsky, Daniela Lozano Casasbuenas, Arman Olfat and Cindi M. Morshead
Biomedicines 2024, 12(3), 663; - 15 Mar 2024
Viewed by 853
Stroke is the leading cause of adult disability worldwide. The majority of stroke survivors are left with devastating functional impairments for which few treatment options exist. Recently, a number of studies have used ectopic expression of transcription factors that direct neuronal cell fate [...] Read more.
Stroke is the leading cause of adult disability worldwide. The majority of stroke survivors are left with devastating functional impairments for which few treatment options exist. Recently, a number of studies have used ectopic expression of transcription factors that direct neuronal cell fate with the intention of converting astrocytes to neurons in various models of brain injury and disease. While there have been reports that question whether astrocyte-to-neuron conversion occurs in vivo, here, we have asked if ectopic expression of the transcription factor Neurod1 is sufficient to promote improved functional outcomes when delivered in the subacute phase following endothelin-1-induced sensory–motor cortex stroke. We used an adeno-associated virus to deliver Neurod1 from the short GFAP promoter and demonstrated improved functional outcomes as early as 28 days post-stroke and persisting to at least 63 days post-stroke. Using Cre-based cell fate tracking, we showed that functional recovery correlated with the expression of neuronal markers in transduced cells by 28 days post-stroke. By 63 days post-stroke, the reporter-expressing cells comprised ~20% of all the neurons in the perilesional cortex and expressed markers of cortical neuron subtypes. Overall, our findings indicate that ectopic expression of Neurod1 in the stroke-injured brain is sufficient to enhance neural repair. Full article
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