Advances in Neurogenesis: 3rd Edition

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: closed (31 March 2025) | Viewed by 3585

Special Issue Editor


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Guest Editor
Life and Health Sciences Research Institute, School of Medicine, Universidade do Minho, Braga, Portugal
Interests: neurogenesis; gliogenesis; epigenetics; transcription factors; depression; neural circuits
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Special Issue Information

Dear Colleagues,

This is the expanded third edition of Advances in Neurogenesis. The first edition led to the publication of 18 papers, while the second edition led to the publication of 10 papers.

The adult brain displays different forms of neural plasticity, ranging from neuronal synapto-dendritic rearrangements to the generation of novel neuronal and glial cells from neural stem cells (NSCs), processes known as adult neuro- and gliogenesis, respectively.

Postnatal neuro- and glioplasticity are largely driven by the transduction of environmental stimuli into essential neuroadaptations. Neuro- and glioplastic maladaptations often result in the manifestation of pathological traits, of which depressive behavior is a paradigmatic example.

Though increasing evidence supports the role of the hippocampal cytogenesis in brain physiology, its precise function is still debatable. The heterogeneity of the experimental models, timeframes, and methodological approaches used to address this subject has yielded conflicting results regarding the impact of the newborn cells on behavior. Still, converging data reveal a role of adult hippocampal cytogenesis in long-term spatial memory, cognitive flexibility, pattern separation, and the clearance of hippocampal memories. Given the involvement of adult neurogenesis in such complex behaviors, it has become plausible to anticipate that its disruption could impact neuronal circuitry and, ultimately, be implicated in the development of psychiatric and neurodegenerative disorders.

Understanding the role of novel genes and cytogenic regulators and better dissecting their impact throughout developmental periods and at different behavioral domains is of paramount importance for increasing our current comprehension of this topic.

Dr. Luisa Alexandra Meireles Pinto
Guest Editor

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Keywords

  • neurogenesis
  • gliogenesis
  • cell plasticity
  • neurophysiology
  • behavior
  • neural circuits
  • cytogenic regulators
  • neuropsychiatric disorders
  • neurodegenerative disorders

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Published Papers (2 papers)

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17 pages, 5031 KiB  
Article
Imipramine, an Acid Sphingomyelinase Inhibitor, Promotes Newborn Neuron Survival in the Hippocampus After Seizure
by Song Hee Lee, Hyun Wook Yang, Beom Seok Kang, Min Kyu Park, Dong Yeon Kim, Hong Ki Song, Hui Chul Choi, Minwoo Lee, Bo Young Choi, Dae-Soon Son and Sang Won Suh
Cells 2025, 14(4), 281; https://doi.org/10.3390/cells14040281 - 14 Feb 2025
Viewed by 772
Abstract
Epilepsy, a chronic neurological disorder, is triggered by various insults, including traumatic brain injury and stroke. Acid sphingomyelinase (ASMase), an enzyme that hydrolyzes sphingomyelin into ceramides, is implicated in oxidative stress, neuroinflammation, and neuronal apoptosis. Ceramides, which have pro-apoptotic properties, contribute to oxidative [...] Read more.
Epilepsy, a chronic neurological disorder, is triggered by various insults, including traumatic brain injury and stroke. Acid sphingomyelinase (ASMase), an enzyme that hydrolyzes sphingomyelin into ceramides, is implicated in oxidative stress, neuroinflammation, and neuronal apoptosis. Ceramides, which have pro-apoptotic properties, contribute to oxidative damage and lysosomal dysfunction, exacerbating neuronal injury. This study investigates the role of ASMase in epilepsy, hypothesizing that seizure activity upregulates ASMase, increasing ceramide levels, DNA damage, and neuronal apoptosis. We employed a pilocarpine-induced rat seizure model and examined the effects of imipramine, an ASMase inhibitor, administered intraperitoneally (10 mg/kg) for four weeks post-seizure induction. Histological and cognitive analyses showed that while imipramine did not prevent early neuronal death within the first week, it significantly reduced markers of neuronal apoptosis by four weeks. Imipramine also promoted hippocampal neurogenesis and preserved cognitive function, which is often impaired following seizures. These findings suggest that ASMase inhibition could mitigate neuronal apoptosis and improve cognitive recovery after seizures. Imipramine may serve as a promising therapeutic strategy for epilepsy-associated neuronal damage and cognitive deficits. Further studies should delineate the molecular mechanisms of ASMase inhibition and evaluate its long-term efficacy in addressing epilepsy-related neurodegeneration and functional impairments. Full article
(This article belongs to the Special Issue Advances in Neurogenesis: 3rd Edition)
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17 pages, 852 KiB  
Review
The Emerging Role of Phosphodiesterase 5 Inhibition in Neurological Disorders: The State of the Art
by Clara Crescioli and Maria Paola Paronetto
Cells 2024, 13(20), 1720; https://doi.org/10.3390/cells13201720 - 17 Oct 2024
Cited by 2 | Viewed by 2427
Abstract
Growing evidence suggests that neuroinflammation is not just a consequence of neurodegeneration in pathologies such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease or Amyotrophic lateral sclerosis, but it is rather a determinant factor, which plays a pivotal role in the onset and progression [...] Read more.
Growing evidence suggests that neuroinflammation is not just a consequence of neurodegeneration in pathologies such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease or Amyotrophic lateral sclerosis, but it is rather a determinant factor, which plays a pivotal role in the onset and progression of these disorders. Neuroinflammation can affect cells and processes in the central nervous system (CNS) as well as immune cells, and might precede protein aggregation, which is a hallmark of the neurodegenerative process. Standard treatment methods are far from being able to counteract inflammation and delay neurodegeneration. Remarkably, phosphodiesterase 5 inhibitors (PDE5is), which represent potent vasoactive drugs used as a first-line treatment for erectile dysfunction (ED), display important anti-inflammatory effects through cyclic guanosine monophosphate (cGMP) level stabilization. Since PDE5 hydrolyzes cGMP, several studies positioned PDE5 as a therapeutic target, and more specifically, PDE5is as potential alternative strategies for the treatment of a variety of neurological disorders. Indeed, PDE5is can limit neuroinflammation and enhance synaptic plasticity, with beneficial effects on cognitive function and memory. The aim of this review is to provide an overview of some of the main processes underlying neuroinflammation and neurodegeneration which may be potential targets for PDE5is, focusing on sildenafil, the most extensively studied. Current strategies using PDEis for the treatment of neurodegenerative diseases will be summarized. Full article
(This article belongs to the Special Issue Advances in Neurogenesis: 3rd Edition)
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