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Cells
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Recent Advances in the Understanding of Neuropsychiatric Illnesses
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Recent Advances in the Understanding of Neuropsychiatric Illnesses

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Neuroscience".

Deadline for manuscript submissions: 15 July 2026 | Viewed by 2023

Special Issue Editors

Dr. Junnan Li

E-Mail Website
Guest Editor
Department of Psychiatry, Johns Hopkins School of Medicine, Baltimore, MD, USA
Interests: intra- and extracellular signaling mechanisms; particularly in the context of neurodegenerative diseases and neuropsychiatric disorders
Dr. Wanli Smith

E-Mail Website
Guest Editor
Cellular Neurobiology Laboratory, Johns Hopkins University, School of Medicine, Baltimore, MD, USA
Interests: Parkinson’s disease; obesity; Alzheimer’s disease; neuronal cell death and protein aggregation in neuropsychiatric conditions
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neuropsychiatric illnesses, encompassing disorders such as schizophrenia, bipolar disorder, Huntington's disease, Alzheimer’s disease, and major depression, pose a significant global health challenge. Despite advances in neuroscience, the molecular and cellular mechanisms driving these conditions—particularly disruptions in intra- and extracellular signaling, synaptic dysfunction, and neuroimmune interactions—remain insufficiently understood. This Special Issue aims to highlight cutting-edge research that bridges basic science with clinical innovation. We invite contributions that offer novel insights into neurodegeneration, neuroinflammation, and circuit-level pathophysiology, as well as studies utilizing emerging tools, such as single-cell omics, CRISPR-based screens, and advanced neuroimaging. Submissions may explore biomarker discovery, therapeutic target validation, or translational strategies designed to improve patient outcomes. By synthesizing multidisciplinary perspectives, this Special Issue strives to catalyze breakthroughs in the understanding and treatment of these complex disorders.

Dr. Junnan Li
Dr. Wanli Smith
Guest Editors

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. Cells 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

  • neuropsychiatric disorders
  • neurodegeneration
  • synaptic plasticity
  • neuroinflammation
  • biomarkers
  • molecular mechanisms
  • translational neuroscience
  • intracellular signaling
  • neuroimaging

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Published Papers (2 papers)

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Research

13 pages, 1759 KB  
Article
The Highly Selective 5-HT2B Receptor Antagonist MW073 Mitigates Aggressive Behavior in an Alzheimer’s Disease Mouse Model
by Erica Acquarone, Saktimayee M. Roy, Agnieszka Staniszewski, Daniel Martin Watterson and Ottavio Arancio
Cells 2026, 15(3), 273; https://doi.org/10.3390/cells15030273 - 1 Feb 2026
Viewed by 701
Abstract
Background: Alzheimer’s disease (AD) is a multifactorial neurodegenerative disorder and the leading cause of dementia worldwide. Progressive synaptic dysfunction underlies declines in cognition, daily functioning, and the development of neuropsychiatric syndromes. Neuropsychiatric syndromes that include agitation and aggression affect 40–60% of patients and [...] Read more.
Background: Alzheimer’s disease (AD) is a multifactorial neurodegenerative disorder and the leading cause of dementia worldwide. Progressive synaptic dysfunction underlies declines in cognition, daily functioning, and the development of neuropsychiatric syndromes. Neuropsychiatric syndromes that include agitation and aggression affect 40–60% of patients and represent a major source of caregiver burden. Serotonin 5-HT2B receptor levels are increased in the AD patient brain, and thus, treatment of AD animal models with the selective 5-HT2B receptor antagonist MW073 in prevention or disease stage paradigms attenuates Aβ- or tau-induced dysfunction. Methods: We investigated the effects of MW073 treatment on the aggressive behavior of Tg2576 mice in a resident–intruder assay. Results: MW073 treatment significantly reduced aggressive behavior in male Tg2576 mice. Conclusions: MW073 efficacy in treating aggression in Tg2576 mice implicates 5-HT2B receptor-mediated signaling in AD neuropsychiatric symptoms as well as cognitive and behavioral dysfunction. Full article
(This article belongs to the Special Issue Recent Advances in the Understanding of Neuropsychiatric Illnesses)
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20 pages, 6255 KB  
Article
Separate BNST Microcircuits Targeted by Direct Versus Amygdala-Relayed Prefrontal Inputs Mediate Dissociable Phenotypes After Isolation
by Hongxia Yuan, Yongmei Zhong and Xuehan Zhang
Cells 2026, 15(2), 116; https://doi.org/10.3390/cells15020116 - 8 Jan 2026
Viewed by 677
Abstract
Anxiety, depression, and social impairment exhibit high clinical comorbidity, yet their underlying shared neural circuitry remains poorly defined. Using a mouse model of chronic social isolation combined with circuit tracing and chemogenetic tools, we identified a key role for the basolateral amygdala (BLA) [...] Read more.
Anxiety, depression, and social impairment exhibit high clinical comorbidity, yet their underlying shared neural circuitry remains poorly defined. Using a mouse model of chronic social isolation combined with circuit tracing and chemogenetic tools, we identified a key role for the basolateral amygdala (BLA) in relaying prefrontal cortex (PFC) signals to the bed nucleus of the stria terminalis (BNST) to drive behavioral changes. Further circuit dissection identified two distinct BNST microcircuits segregated by their input sources: one receives indirect PFC input relayed through the BLA (PFC → BLA → BNST), while the other is innervated by direct PFC projections (PFC → BNST). Chemogenetic inhibition of BLA neurons in the indirect pathway ameliorated anxiety-like behavior, depression-like behavior, and social deficits. Within the BNST, however, inhibition of neurons in PFC → BLA → BNST pathway selectively alleviated affective phenotypes without altering social behavior. In contrast, inhibition of neurons in PFC → BNST pathway specifically restored social recognition while leaving emotional behaviors intact. Thus, the BLA integrates PFC-derived signals to broadly modulate behavior, while downstream BNST microcircuits dissociate these influences. The indirect, BLA-relayed pathway within the BNST specifically drives affective symptoms, whereas the direct PFC → BNST pathway selectively governs social recognition. This dissociable circuit model offers a new framework for understanding clinical comorbidity and may inform targeted interventions for distinct symptom dimensions. Full article
(This article belongs to the Special Issue Recent Advances in the Understanding of Neuropsychiatric Illnesses)
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