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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 August 2026 | Viewed by 64500

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 Issues, Collections and Topics in MDPI journals

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 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. Biology is an international peer-reviewed open access semimonthly 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 (7 papers)

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Research

Jump to: Review

13 pages, 561 KB  
Article
Effects of Apical Dendrite Integrity on Action Potential Properties in Layer 6 Corticothalamic Pyramidal Neurons: Evidence for Hemispheric Differences
by Ahmed A. Aldohbeyb
Biology 2026, 15(8), 608; https://doi.org/10.3390/biology15080608 - 12 Apr 2026
Viewed by 558
Abstract
Hemispheric asymmetries in the cortical structure and function are well documented, but whether this asymmetry is reflected in the electrophysiological properties of the same neuron type remains unclear, particularly given the many factors that influence action potential (AP) generation. Among these factors, dendritic [...] Read more.
Hemispheric asymmetries in the cortical structure and function are well documented, but whether this asymmetry is reflected in the electrophysiological properties of the same neuron type remains unclear, particularly given the many factors that influence action potential (AP) generation. Among these factors, dendritic tree size plays a crucial role in AP generation and in forward and backward propagation, yet it is not well understood whether dendritic size affects spike generation similarly in the two hemispheres. Here, electrophysiological recordings of layer 6a corticothalamic (CT) pyramidal neurons from a mouse’s left and right primary visual cortex were analyzed to examine how apical dendrite integrity influences somatic AP properties. Neurons were divided into four groups based on hemisphere and apical dendrite status (intact vs. truncated), and the AP shape parameters were quantified in response to current stimulation. Intact CT neurons showed similar AP rapidity and width across hemispheres but differed in AP threshold and amplitude. In contrast, a comparison of the intact and truncated neurons within each hemisphere revealed significant and opposing effects of apical dendrite truncation on all AP parameters. These results suggest that the coupling between dendritic morphology and somatic AP generation differs between hemispheres, implying distinct rules for integrating dendritic load in the left and right CT neurons. Full article
(This article belongs to the Special Issue Young Researchers in Neuroscience)
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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 1261
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

Jump to: Research

35 pages, 6168 KB  
Review
Diabetic Peripheral Neuropathy: Mechanisms and Emerging Therapies
by Mohammed M. H. Albariqi, Ibrahim A. Alradwan, Saad M. Alqahtani, Majed A. Majrashi, Basem Jahz Almutiri, Amjad Jabaan and Sultan Alzahrani
Biology 2026, 15(9), 723; https://doi.org/10.3390/biology15090723 - 2 May 2026
Viewed by 1077
Abstract
Diabetic peripheral neuropathy (DPN) is a common and debilitating complication of diabetes mellitus which affects individuals with both type 1 and type 2 diabetes mellitus (T2DM), presenting with sensory loss, pain, and progressive nerve dysfunction. DPN pathogenesis is multifactorial: chronic hyperglycemia activates the [...] Read more.
Diabetic peripheral neuropathy (DPN) is a common and debilitating complication of diabetes mellitus which affects individuals with both type 1 and type 2 diabetes mellitus (T2DM), presenting with sensory loss, pain, and progressive nerve dysfunction. DPN pathogenesis is multifactorial: chronic hyperglycemia activates the polyol, hexosamine, and protein kinase C (PKC) pathways, increases advanced glycation end-products, and drives oxidative stress, mitochondrial dysfunction, inflammation, and impaired neurotrophic signaling. In addition to hyperglycemia-driven mechanisms, dyslipidemia and microvascular insufficiency exacerbate neural ischemia and metabolic stress. Recent mechanistic, animal, and associative human studies further implicate amyloidogenic toxicity, particularly from human islet amyloid polypeptide (hIAPP), as a plausible contributory factor in peripheral nerve degeneration in T2DM, linking protein misfolding and aggregation to axonal damage and demyelination in DPN. Despite increased understanding of these mechanisms, current treatments remain mainly symptomatic. Emerging therapeutic strategies, including antioxidants, anti-inflammatory agents, modulators of mitochondrial function, amyloid oligomer modulators, neurotrophic enhancers, and regenerative approaches such as stem cells and gene-based therapies, offer potential to modify disease progression. The strength of evidence across these methods varies, ranging from mechanistic and animal studies to early human research and, in some cases, randomized clinical trials. Therefore, although several candidates show potential to alter the disease, few have demonstrated consistent benefits on objective measures of nerve structure or function in large clinical trials. This review summarizes the key mechanisms driving DPN in T2DM and highlights promising therapeutic innovations poised for clinical translation. Full article
(This article belongs to the Special Issue Young Researchers in Neuroscience)
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33 pages, 1777 KB  
Review
Cancer Neuroscience: Linking Neuronal Plasticity with Brain Tumor Growth and Resistance
by Doaa S. R. Khafaga, Youssef Basem, Hager Mohamed AlAtar, Abanoub Sherif, Alamer Ata, Fayek Sabry, Manar T. El-Morsy and Shimaa S. Attia
Biology 2026, 15(2), 108; https://doi.org/10.3390/biology15020108 - 6 Jan 2026
Viewed by 2634
Abstract
Brain tumors, particularly glioblastoma, remain among the most lethal cancers, with limited survival benefits from current genetic and molecular-targeted approaches. Emerging evidence reveals that beyond oncogenes and mutations, neuronal plasticity, long-term potentiation, synaptic remodeling, and neurotransmitter-driven signaling play a pivotal role in shaping [...] Read more.
Brain tumors, particularly glioblastoma, remain among the most lethal cancers, with limited survival benefits from current genetic and molecular-targeted approaches. Emerging evidence reveals that beyond oncogenes and mutations, neuronal plasticity, long-term potentiation, synaptic remodeling, and neurotransmitter-driven signaling play a pivotal role in shaping tumor progression and therapeutic response. This convergence of neuroscience and oncology has given rise to the field of cancer neuroscience, which explores the bidirectional interactions between neurons and malignant cells. In this review, we summarize fundamental principles of neuronal plasticity, contrasting physiological roles with pathological reprogramming in brain tumors. We highlight how tumor cells exploit synaptic input, particularly glutamatergic signaling, to enhance proliferation, invasion, and integration into neural circuits. We further discuss how neuronal-driven feedback loops contribute to therapy resistance, including chemoresistance, radioresistance, and immune evasion, mediated through pathways such as mitogen-activated protein kinase (MAPK), phosphoinositide 3-kinase/protein kinase B (PI3K/AKT), and calcium influx. The tumor microenvironment, including astrocytes, microglia, and oligodendrocyte-lineage cells, emerges as an active participant in reinforcing this neuron-tumor ecosystem. Finally, this review explores therapeutic opportunities targeting neuronal plasticity, spanning pharmacological interventions, neuromodulation approaches (transcranial magnetic stimulation (TMS), deep brain stimulation (DBS), optogenetics), and computational/artificial intelligence frameworks that model neuron tumor networks to predict personalized therapy. Also, we propose future directions integrating connect omics, neuroinformatics, and brain organoid models to refine translational strategies. Full article
(This article belongs to the Special Issue Young Researchers in Neuroscience)
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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
Cited by 5 | Viewed by 3423
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 35 | Viewed by 43070
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 11 | Viewed by 11334
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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