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Involvement of Neuroinflammatory Processes in Psychiatric Conditions

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 March 2025 | Viewed by 2158

Special Issue Editor


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Guest Editor
1. Group of Cellular and Molecular Pharmacology, Department of Pharmacology, University of Murcia, 30120 Murcia, Spain
2. Instituto Murciano de Investigación Biosanitaria (IMIB), 30120 Murcia, Spain
Interests: biomedical science; molecular neuroscience; neuropharmacology; neurobiology; behavioral pharmacology; brain anatomy; brain connectivity; neuroimmunology; learning and memory; drug addiction

Special Issue Information

Dear Colleagues,

Psychiatric disorders alter an individual's cognition, emotional regulation or behavior, and constitute a major socioeconomic and health burden worldwide. For a long time, the impairments underlying psychiatric disorders were considered to affect neuronal cells exclusively. Nonetheless, neuroinflammation is nowadays gaining attention as a pivotal factor in mental conditions. This dynamic process encompasses, microglial and astrocytic alterations, and cytokine and chemokine fluctuations within the central nervous system, among other mechanisms, known to modulate learning and memory, motivation and behavior, amidst other functions. Exploring inflammatory alterations in key brain areas associated with these conditions could serve for the identification of new biomarkers useful for the prevention and diagnosis of psychiatric disorders, as well as for the development of effective neuromodulation therapies.

Lead by Dr. Cristina Núñez and assisted by our Topical Advisory Panel Member Dr. Victoria Gomez-Murcia (University of Murcia & Instituto Murciano de Investigación Biosanitaria (IMIB)), this Special Issue will be centered on the neuroinflammatory aspects of mental conditions in a broad context, including biochemical, genetic, morphological or functional aspects, but also various interventions for their treatment that alleviate inflammatory processes in the brain. Continued research at the intersection of neuroinflammation and psychiatry will contribute to both prevent and provide precise diagnostic and therapeutic approaches to address neuropsychiatric disorders. 

Dr. Cristina Núñez
Guest Editor

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Keywords

  • neuroinflammation
  • glia
  • chemokine
  • cytokine
  • psychiatry disorder
  • motivation
  • learning
  • behavior
  • mental illness
  • psychopharmacology

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Published Papers (1 paper)

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Research

17 pages, 3822 KiB  
Article
Postnatal Allergic Inhalation Induces Glial Inflammation in the Olfactory Bulb and Leads to Autism-Like Traits in Mice
by Eizo Tanaka, Ryo Yamasaki, Ban-yu Saitoh, Amina Abdelhadi, Satoshi Nagata, Sato Yoshidomi, Yuka Inoue, Koichiro Matsumoto, Jun-ichi Kira and Noriko Isobe
Int. J. Mol. Sci. 2024, 25(19), 10464; https://doi.org/10.3390/ijms251910464 - 28 Sep 2024
Viewed by 1075
Abstract
Autism spectrum disorder (ASD) is one of the most prevalent neurodevelopmental disorders. To explore its pathophysiology, we investigated the association between neonatal allergic exposure and behavioral changes. Adult female C57BL/6J mice were immunized with adjuvant (aluminum hydroxide) or ovalbumin emulsified with adjuvant. After [...] Read more.
Autism spectrum disorder (ASD) is one of the most prevalent neurodevelopmental disorders. To explore its pathophysiology, we investigated the association between neonatal allergic exposure and behavioral changes. Adult female C57BL/6J mice were immunized with adjuvant (aluminum hydroxide) or ovalbumin emulsified with adjuvant. After immunization, the mice were mated, and offspring were born at full term. The postnatal dams and infants were then simultaneously exposed to an allergen (ovalbumin) or vehicle via inhalation. After weaning, behavioral testing and histopathological analyses were conducted on male offspring. Compared with the vehicle-exposed offspring, the ovalbumin-exposed offspring had decreased sociability and increased repetitive behavior, thus representing an ASD-like phenotype in mice. Moreover, histopathological analyses revealed that the ovalbumin-exposed mice had increased astroglial, microglial, and eosinophilic infiltration in the olfactory bulb, as well as increased eosinophils in the nasal mucosa. The ovalbumin-exposed mice also had decreased dendritic spine density and a lower proportion of mature spines, suggesting the impairment of stimulus-induced synaptogenesis. In conclusion, postnatal allergic exposure induced an ASD-like phenotype, as well as allergic rhinitis, which was followed by glial inflammation in the olfactory bulb parenchyma. Full article
(This article belongs to the Special Issue Involvement of Neuroinflammatory Processes in Psychiatric Conditions)
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