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Biology
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Young Researchers in Neuroscience
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Young Researchers in Neuroscience

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Neuroscience".

Deadline for manuscript submissions: 31 October 2025 | Viewed by 26154

Special Issue Editor

Prof. Dr. Yansheng Du

E-Mail Website
Guest Editor
Department of Neurology, Indiana University School of Medicine, Indianapolis, IN 46202, USA
Interests: neurology

Special Issue Information

Dear Colleagues,

In this Special Issue, we aim to feature early-career researchers in neuroscience. The senior author(s) of each contribution should be (a) the first or last author and the corresponding author, and (b) have completed their Ph.D in the last 10 years (or equivalent), be an assistant professor, or be on track to receive tenure. We welcome submissions from a range of research fields. Articles submitted to this Special Issue should meet all standard requirements of individual biology articles (regarding quality, novelty, and significance) and be relevant to a broad international and interdisciplinary readership.

Authors contributing to this Special Issue will have the opportunity to be nominated for next year's Young Investigator Award.

Prof. Dr. Yansheng Du
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. Biology is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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

  • neurobiology
  • cell biology
  • molecular mechanisms
  • neural development
  • synaptic function
  • ion channels
  • neurotransmitter systems
  • gene expression
  • neuronal signaling
  • cellular physiology

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (4 papers)

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Research

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21 pages, 4743 KB  
Article
Transcriptomic Investigation of FoxM1-Mediated Neuroprotection by hAEC-Derived Exosomes in an In Vitro Ischemic Stroke Model
by Dong Wang, Jiaxin Liu, Liang Wu, Xiubao Yang, Zhihao Fang, Zhong Sun and Dong Chen
Biology 2025, 14(10), 1368; https://doi.org/10.3390/biology14101368 - 7 Oct 2025
Viewed by 334
Abstract
Human amniotic epithelial cell-derived exosomes (hAECs-Exos) are nanoscale extracellular vesicles with neuroprotective, regenerative, and anti-inflammatory properties, presenting a promising cell-free therapeutic approach for ischemic stroke. This study investigated the protective effects of hAECs-Exos against ischemic injury and explored the underlying molecular mechanisms. An [...] Read more.
Human amniotic epithelial cell-derived exosomes (hAECs-Exos) are nanoscale extracellular vesicles with neuroprotective, regenerative, and anti-inflammatory properties, presenting a promising cell-free therapeutic approach for ischemic stroke. This study investigated the protective effects of hAECs-Exos against ischemic injury and explored the underlying molecular mechanisms. An optimized oxygen-glucose deprivation/reoxygenation (OGD/R) model was established in murine hippocampal HT22 neurons and BV2 microglial cells to simulate ischemic conditions. hAECs-Exos were successfully isolated and characterized via transmission electron microscopy, nanoparticle tracking analysis, and Western blotting. Confocal microscopy confirmed efficient exosome uptake by both cell types. Functional analyses revealed that hAECs-Exos significantly improved cell viability, suppressed pro-inflammatory cytokine release, alleviated oxidative stress, and modulated apoptosis-related proteins. RNA sequencing identified Forkhead box protein M1 (FoxM1) as a significantly upregulated transcription factor following hAECs-Exos treatment. Further experiments demonstrated that knockdown of FoxM1 in hAECs abolished the beneficial effects of exosomes on the viability of HT22 and BV2 cells and on the suppression of inflammation, oxidative stress, and apoptosis. These findings indicate that hAECs-Exos confer neuroprotection through FoxM1-dependent mechanisms. Together, our results highlight the therapeutic potential of hAECs-Exos as a safe, effective, and clinically translatable strategy for ischemic stroke treatment, warranting future validation in vivo and rescue experiments to fully elucidate FoxM1’s causal role. Full article
(This article belongs to the Special Issue Young Researchers in Neuroscience)
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Review

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37 pages, 2512 KB  
Review
Microglial Autophagy and Mitophagy in Ischemic Stroke: From Dual Roles to Therapeutic Modulation
by Juan Wu, Jiaxin Liu, Yanwen Li, Fang Du, Weijia Li, Karuppiah Thilakavathy, Jonathan Chee Woei Lim, Zhong Sun and Juqing Deng
Biology 2025, 14(9), 1269; https://doi.org/10.3390/biology14091269 - 15 Sep 2025
Viewed by 741
Abstract
Ischemic stroke induces complex neuroinflammatory cascades, where microglial autophagy and mitophagy serve dual roles in both injury amplification and tissue repair. This scoping review synthesized current evidence on their regulatory mechanisms and therapeutic implications. Literature was identified via PubMed and Embase, yielding 79 [...] Read more.
Ischemic stroke induces complex neuroinflammatory cascades, where microglial autophagy and mitophagy serve dual roles in both injury amplification and tissue repair. This scoping review synthesized current evidence on their regulatory mechanisms and therapeutic implications. Literature was identified via PubMed and Embase, yielding 79 records, from which 39 original research articles and 13 review papers were included after eligibility screening. Search terms included “microglia,” “autophagy,” and “ischemic stroke.” Protective autophagy was frequently associated with AMPK activation, mTOR inhibition, and mitophagy pathways such as PINK1/Parkin and BNIP3/NIX, facilitating mitochondrial clearance, M2 polarization, and anti-inflammatory signaling. Therapeutic agents such as rapamycin, Tat-Beclin 1, and Urolithin A consistently demonstrated neuroprotection in preclinical stroke models. In contrast, excessive or prolonged autophagic activation was linked to inflammasome amplification, oxidative stress, and phagoptosis. Limited human studies reported associations between elevated serum ATG5 levels or ATG7 polymorphisms and worse clinical outcomes, suggesting preliminary translational relevance. These findings support the potential of phase-specific modulation of microglial autophagy as a therapeutic avenue for stroke, although further validation in human models and development of autophagy biomarkers are needed for clinical application. Full article
(This article belongs to the Special Issue Young Researchers in Neuroscience)
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37 pages, 3254 KB  
Review
The Journey of the Default Mode Network: Development, Function, and Impact on Mental Health
by Felipe Rici Azarias, Gustavo Henrique Doná Rodrigues Almeida, Luana Félix de Melo, Rose Eli Grassi Rici and Durvanei Augusto Maria
Biology 2025, 14(4), 395; https://doi.org/10.3390/biology14040395 - 10 Apr 2025
Cited by 4 | Viewed by 18476
Abstract
The Default Mode Network has been extensively studied in recent decades due to its central role in higher cognitive processes and its relevance for understanding mental disorders. This neural network, characterized by synchronized and coherent activity at rest, is intrinsically linked to self-reflection, [...] Read more.
The Default Mode Network has been extensively studied in recent decades due to its central role in higher cognitive processes and its relevance for understanding mental disorders. This neural network, characterized by synchronized and coherent activity at rest, is intrinsically linked to self-reflection, mental exploration, social interaction, and emotional processing. Our understanding of the DMN extends beyond humans to non-human animals, where it has been observed in various species, highlighting its evolutionary basis and adaptive significance throughout phylogenetic history. Additionally, the DMN plays a crucial role in brain development during childhood and adolescence, influencing fundamental cognitive and emotional processes. This literature review aims to provide a comprehensive overview of the DMN, addressing its structural, functional, and evolutionary aspects, as well as its impact from infancy to adulthood. By gaining a deeper understanding of the organization and function of the DMN, we can advance our knowledge of the neural mechanisms that underlie cognition, behavior, and mental health. This, in turn, can lead to more effective therapeutic strategies for a range of neuropsychiatric conditions. Full article
(This article belongs to the Special Issue Young Researchers in Neuroscience)
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42 pages, 4503 KB  
Review
Advances in Huntington’s Disease Biomarkers: A 10-Year Bibliometric Analysis and a Comprehensive Review
by Sarah Aqel, Jamil Ahmad, Iman Saleh, Aseela Fathima, Asmaa A. Al Thani, Wael M. Y. Mohamed and Abdullah A. Shaito
Biology 2025, 14(2), 129; https://doi.org/10.3390/biology14020129 - 26 Jan 2025
Cited by 4 | Viewed by 5840
Abstract
Neurodegenerative disorders (NDs) cause progressive neuronal loss and are a significant public health concern, with NDs projected to become the second leading global cause of death within two decades. Huntington’s disease (HD) is a rare, progressive ND caused by an autosomal-dominant mutation in [...] Read more.
Neurodegenerative disorders (NDs) cause progressive neuronal loss and are a significant public health concern, with NDs projected to become the second leading global cause of death within two decades. Huntington’s disease (HD) is a rare, progressive ND caused by an autosomal-dominant mutation in the huntingtin (HTT) gene, leading to severe neuronal loss in the brain and resulting in debilitating motor, cognitive, and psychiatric symptoms. Given the complex pathology of HD, biomarkers are essential for performing early diagnosis, monitoring disease progression, and evaluating treatment efficacy. However, the identification of consistent HD biomarkers is challenging due to the prolonged premanifest HD stage, HD’s heterogeneous presentation, and its multiple underlying biological pathways. This study involves a 10-year bibliometric analysis of HD biomarker research, revealing key research trends and gaps. The study also features a comprehensive literature review of emerging HD biomarkers, concluding the need for better stratification of HD patients and well-designed longitudinal studies to validate HD biomarkers. Promising candidate wet HD biomarkers— including neurofilament light chain protein (NfL), microRNAs, the mutant HTT protein, and specific metabolic and inflammatory markers— are discussed, with emphasis on their potential utility in the premanifest HD stage. Additionally, biomarkers reflecting brain structural deficits and motor or behavioral impairments, such as neurophysiological (e.g., motor tapping, speech, EEG, and event-related potentials) and imaging (e.g., MRI, PET, and diffusion tensor imaging) biomarkers, are evaluated. The findings underscore that the discovery and validation of reliable HD biomarkers urgently require improved patient stratification and well-designed longitudinal studies. Reliable biomarkers, particularly in the premanifest HD stage, are crucial for optimizing HD clinical management strategies, enabling personalized treatment approaches, and advancing clinical trials of HD-modifying therapies. Full article
(This article belongs to the Special Issue Young Researchers in Neuroscience)
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