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Neurogenesis and Neurodegeneration: Insights into Regeneration and the Impact of Neurotrophins

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 2026 | Viewed by 5174

Special Issue Editor

Dr. Eva Terzibasi Tozzini

E-Mail Website
Guest Editor
Biology and Evolution of Marine Organisms Department (BEOM), Stazione Zoologica Anton Dohrn, 80121 Napoli, Italy
Interests: adult neurogenesis; aging; neurodegeneration; teleost animal models marine vertebrates; neurotrophins; immunohistochemistri; in situ hybridization
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

Our Special Issue, "Neurogenesis and Neurodegeneration: Insights into Regeneration and the Impact of Neurotrophins", aims to showcase cutting-edge research that illuminates the complex relationship between the birth of new neurons and the progressive loss of existing ones—processes that are fundamentally linked to brain health, disease, and therapeutic intervention. 

We encourage scientists worldwide to submit original research articles, comprehensive reviews, and insightful perspectives that explore the intricate mechanisms that drive neurogenesis, with a particular focus on the critical role of neurotrophins. We welcome studies that explore regenerative strategies for neurodegenerative disorders, including those that consider the impact of environmental factors and genetic predisposition on both neurogenesis and neurodegeneration.

Leading by Dr. Eva Terzibasi Tozzini and assisting by Dr. Sara Bagnoli (Biology Laboratory (BIO@SNS), Scuola Normale Superiore, Italy), this Special Issue aims to provide a comprehensive platform for advances in the understanding of brain plasticity, repair mechanisms, and promising therapeutic avenues. 

Submit your work and help shape the future of neurogenesis, neurodegeneration, and regeneration research! We look forward to receiving your submission.

Dr. Eva Terzibasi Tozzini
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 250 words) can be sent to the Editorial Office for assessment.

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
  • neurodegeneration and regeneration
  • neurotrophins
  • brain plasticity

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Published Papers (2 papers)

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Review

50 pages, 3304 KB  
Review
Perspective for Modulation of Hypothalamic Neurogenesis: Integrating Anatomical Insights with Exercise and Dietary Interventions
by Javier Choquet de Isla, Manuel Bández-Ruiz, Ignacio Rosety-Rodríguez, Inmaculada Pérez-López, Miguel Ángel Rosety-Rodríguez, Cristina Verástegui-Escolano, Ismael Sánchez-Gomar and Noelia Geribaldi-Doldán
Int. J. Mol. Sci. 2025, 26(22), 10914; https://doi.org/10.3390/ijms262210914 - 11 Nov 2025
Viewed by 1379
Abstract
Adult neurogenesis is well established in canonical niches—the dentate gyrus and the subventricular zone, where aerobic exercise reliably enhances progenitor proliferation, survival, and synaptic integration via increased cerebral blood flow, neurotrophins (e.g., BDNF, IGF-1), neurotransmitter regulation, and reduced neuroinflammation. Nutraceuticals (e.g., polyphenols, omega-3, [...] Read more.
Adult neurogenesis is well established in canonical niches—the dentate gyrus and the subventricular zone, where aerobic exercise reliably enhances progenitor proliferation, survival, and synaptic integration via increased cerebral blood flow, neurotrophins (e.g., BDNF, IGF-1), neurotransmitter regulation, and reduced neuroinflammation. Nutraceuticals (e.g., polyphenols, omega-3, creatine, vitamins) further support neuroplasticity and neuronal survival through convergent trophic, anti-inflammatory, and metabolic pathways. By contrast, the hypothalamus, a metabolically pivotal, non-canonical niche, remains comparatively understudied. Here, we synthesize anatomical and functional features of hypothalamic neural stem cells, primarily tanycytes (α1, α2, β1, β2), which line the third ventricle and differentially contribute to neuronal activity regulation, metabolic signaling, and cerebrospinal fluid–portal vasculature coupling, thereby linking neurogenesis to endocrine control. Notably, tanycytes can form neurospheres in vitro, enabling mechanistic interrogation. Although evidence for adult hypothalamic neurogenesis in humans is debated due to methodological constraints, animal data suggest potential relevance to disorders characterized by neuronal loss, metabolic dysregulation, and impaired neuroendocrine function. We propose that an integrative framework is timely: exercise and diet likely interact in the hypothalamic niche through shared mediators (BDNF, IGF-1, CNTF, GPR40) and exercise-derived signals (e.g., lactate, IL-6) that may be complemented by defined nutraceuticals. Yet critical uncertainties persist, including the extent of bona fide hypothalamic neurogenesis, nucleus-specific responses (arcuate nucleus, paraventricular nucleus, ventromedial hypothalamic nucleus), and the mechanistic integration of lifestyle signals in this region. To address these gaps, we outline actionable priorities: (i) single-cell and lineage-tracing studies of tanycyte subtypes under distinct training modalities (aerobic, high-intensity interval training, resistance); (ii) combinatorial interventions pairing structured exercise with nutraceuticals to test synergy on progenitor dynamics and inflammation; and (iii) multi-omics and translational studies to identify biomarkers and establish clinical relevance. Clarifying these interactions will determine whether lifestyle and supplementation strategies can synergistically modulate hypothalamic neurogenesis and inform therapies for neurological, neuropsychiatric, and metabolic disorders. Full article
(This article belongs to the Special Issue Neurogenesis and Neurodegeneration: Insights into Regeneration and the Impact of Neurotrophins)
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24 pages, 1404 KB  
Review
Hippocampal Neurogenesis in Alzheimer’s Disease: Multimodal Therapeutics and the Neurogenic Impairment Index Framework
by Li Ma, Qian Wei, Ming Jiang, Yanyan Wu, Xia Liu, Qinghu Yang, Zhantao Bai and Liang Yang
Int. J. Mol. Sci. 2025, 26(13), 6105; https://doi.org/10.3390/ijms26136105 - 25 Jun 2025
Viewed by 3512
Abstract
Alzheimer’s disease (AD) is characterized by progressive cognitive decline strongly associated with impaired adult hippocampal neurogenesis (AHN). Mounting evidence suggests that this impairment results from both the intrinsic dysfunction of neural stem cells (NSCs)—such as transcriptional alterations in quiescent states—and extrinsic niche disruptions, [...] Read more.
Alzheimer’s disease (AD) is characterized by progressive cognitive decline strongly associated with impaired adult hippocampal neurogenesis (AHN). Mounting evidence suggests that this impairment results from both the intrinsic dysfunction of neural stem cells (NSCs)—such as transcriptional alterations in quiescent states—and extrinsic niche disruptions, including the dysregulation of the Reelin signaling pathway and heightened neuroinflammation. Notably, AHN deficits may precede classical amyloid-β and Tau pathology, supporting their potential as early biomarkers of disease progression. In this review, we synthesize recent advances in therapeutic strategies aimed at restoring AHN, encompassing pharmacological agents, natural products, and non-pharmacological interventions such as environmental enrichment and dietary modulation. Emerging approaches—including BDNF-targeted nanocarriers, NSC-derived extracellular vesicles, and multimodal lifestyle interventions—highlight the translational promise of enhancing neurogenesis in models of familial AD. We further propose the Neurogenesis Impairment Index (NII)—a novel composite metric that quantifies hippocampal neurogenic capacity relative to amyloid burden, while adjusting for demographic and cognitive variables. By integrating neurogenic potential, cognitive performance, and pathological load, NII provides a framework for stratifying disease severity and guiding personalized therapeutic approaches. Despite ongoing challenges—such as interspecies differences in neurogenesis rates and the limitations of stem cell-based therapies—this integrative perspective offers a promising avenue to bridge mechanistic insights with clinical innovation in the development of next-generation AD treatments. Full article
(This article belongs to the Special Issue Neurogenesis and Neurodegeneration: Insights into Regeneration and the Impact of Neurotrophins)
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