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New Advances in Drug-Induced Neurogenesis
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New Advances in Drug-Induced Neurogenesis

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 June 2025 | Viewed by 2765

Special Issue Editor

Dr. Tiago Santos

E-Mail Website
Guest Editor
School of Medicine, University of Minho, 4710-057 Braga, Portugal
Interests: brain delivery; blood-brain barrier; central nervous system; neuroblasts; olfactory bulb; angiopep-2

Special Issue Information

Dear Colleagues,

New neurons are generated in the mammalian brain throughout adulthood, primarily in the subventricular zone (SVZ) and the hippocampal subgranular zone (SGZ). However, recent studies have revealed the existence of neurogenesis in other brain regions, including the cortex, substantia nigra, and hypothalamus. These findings emphasize the broad neurogenic potential of the brain, which can be attributed to the presence of stem/progenitor cells and the migration of neuroblasts. Understanding the intricate interplay between drugs and neural stem cells is crucial for unlocking the therapeutic potential of neurogenesis in treating various neurological conditions such as neurodegenerative diseases, epilepsy, stroke, cognitive impairment and dementia, depression and anxiety disorders, spinal cord injury, and traumatic brain injury.

This Special Issue seeks to shed light on the latest advancements in drug-induced neurogenesis and provide valuable insights into regenerative medicine. Specifically, it will explore the clinical translational potential, mechanisms and pathways involved and delve into innovative drug delivery systems. Altogether, this issue aims to pave the way for safer and more efficient approaches to harnessing the potential of drug-induced neurogenesis for regenerative medicine applications. Your valuable contribution will further advance our knowledge in this field and potentially lead to transformative therapies for neurological disorders.

Dr. Tiago Santos
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • neurogenesis
  • neural stem cells
  • neurogenic niches
  • subventricular zone
  • subgranular zone
  • regeneration
  • neurodegenerative diseases
  • drug delivery systems

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Published Papers (2 papers)

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Research

30 pages, 5956 KiB  
Article
Neuroprotective Effects of VEGF-B in a Murine Model of Aggressive Neuronal Loss with Childhood Onset
by Laura Pérez-Revuelta, David Pérez-Boyero, Ester Pérez-Martín, Valeria Lorena Cabedo, Pablo González Téllez de Meneses, Eduardo Weruaga, David Díaz and José Ramón Alonso
Int. J. Mol. Sci. 2025, 26(2), 538; https://doi.org/10.3390/ijms26020538 - 10 Jan 2025
Viewed by 458
Abstract
In recent decades, the scientific community has faced a major challenge in the search for new therapies that can slow down or alleviate the process of neuronal death that accompanies neurodegenerative diseases. This study aimed to identify an effective therapy using neurotrophic factors [...] Read more.
In recent decades, the scientific community has faced a major challenge in the search for new therapies that can slow down or alleviate the process of neuronal death that accompanies neurodegenerative diseases. This study aimed to identify an effective therapy using neurotrophic factors to delay the rapid and aggressive cerebellar degeneration experienced by the Purkinje Cell Degeneration (PCD) mouse, a model of childhood-onset neurodegeneration with cerebellar atrophy (CONDCA). Initially, we analyzed the changes in the expression of several neurotrophic factors related to the degenerative process itself, identifying changes in insulin-like growth factor 1 (IGF-1) and Vascular Endothelial Growth Factor B (VEGF-B) in the affected animals. Then, we administered pharmacological treatments using human recombinant IGF-1 (rhIGF-1) or VEGF-B (rhVEGF-B) proteins, considering their temporal variations during the degenerative process. The effects of these treatments on motor, cognitive, and social behavior, as well as on cerebellar destructuration were analyzed. Whereas treatment with rhIGF-1 did not demonstrate any neuroprotective effect, rhVEGF-B administration at moderate dosages stopped the process of neuronal death and restored motor, cognitive, and social functions altered in PCD mice (and CONDCA patients). However, increasing the frequency of rhVEGF-B administration had a detrimental effect on Purkinje cell survival, suggesting an inverted U-shaped dose–response curve of this substance. Additionally, we demonstrate that this neuroprotective effect was achieved through a partial inhibition or delay of apoptosis. These findings provide strong evidence supporting the use of rhVEGF-B as a pharmacological agent to limit severe cerebellar neurodegenerative processes. Full article
(This article belongs to the Special Issue New Advances in Drug-Induced Neurogenesis)
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17 pages, 6935 KiB  
Article
Inhibition of Apoptosis in a Model of Ischemic Stroke Leads to Enhanced Cell Survival, Endogenous Neural Precursor Cell Activation and Improved Functional Outcomes
by Rehnuma Islam, Jan-Eric Ahlfors, Ricky Siu, Humna Noman, Roya Akbary and Cindi M. Morshead
Int. J. Mol. Sci. 2024, 25(3), 1786; https://doi.org/10.3390/ijms25031786 - 1 Feb 2024
Cited by 2 | Viewed by 1717
Abstract
Stroke results in neuronal cell death, which causes long-term disabilities in adults. Treatment options are limited and rely on a narrow window of opportunity. Apoptosis inhibitors demonstrate efficacy in improving neuronal cell survival in animal models of stroke. However, many inhibitors non-specifically target [...] Read more.
Stroke results in neuronal cell death, which causes long-term disabilities in adults. Treatment options are limited and rely on a narrow window of opportunity. Apoptosis inhibitors demonstrate efficacy in improving neuronal cell survival in animal models of stroke. However, many inhibitors non-specifically target apoptosis pathways and high doses are needed for treatment. We explored the use of a novel caspase-3/7 inhibitor, New World Laboratories (NWL) 283, with a lower IC50 than current caspase-3/7 inhibitors. We performed in vitro and in vivo assays to determine the efficacy of NWL283 in modulating cell death in a preclinical model of stroke. In vitro and in vivo assays show that NWL283 enhances cell survival of neural precursor cells. Delivery of NWL283 following stroke enhances endogenous NPC migration and leads to increased neurogenesis in the stroke-injured cortex. Furthermore, acute NWL283 administration is neuroprotective at the stroke injury site, decreasing neuronal cell death and reducing microglia activation. Coincident with NWL283 delivery for 8 days, stroke-injured mice exhibited improved functional outcomes that persisted following cessation of the drug. Therefore, we propose that NWL283 is a promising therapeutic warranting further investigation to enhance stroke recovery. Full article
(This article belongs to the Special Issue New Advances in Drug-Induced Neurogenesis)
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