Neuroinflammation in Neuropsychiatric Disorders

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Psychiatric Diseases".

Deadline for manuscript submissions: 31 August 2024 | Viewed by 1692

Special Issue Editor

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Guest Editor
1. Department of Neurology, College of Medicine, University of Tennessee Health Science Center, Memphis, TN, USA
2. Center for Muscle, Metabolism and Neuropathology, Division of Regenerative and Rehabilitation Sciences, College of Health Professions, University of Tennessee Health Science Center, Memphis, TN, USA
Interests: Alzheimer’s disease; Parkinson’s disease; neurodevelopmental disorders; DNA damage; neuroinflammation; oxidative stress and antioxidants; gut-brain axis; long noncoding RNAs
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Special Issue Information

Dear Colleagues,

Several studies suggest that inflammation plays a critical role in the onset and progression of multiple neuropsychiatric disorders in children, adults, and older adults, such as bipolar disorder, autism spectrum disorder (ASD), developmental coordination disorders (DCDs), anxiety disorders, post-traumatic stress disorder, schizophrenia and neurodegenerative diseases. Neuropsychiatric symptoms are also common following traumatic brain injury (TBI), and neuroinflammatory responses are suggested to be the main culprit behind the neuropsychiatric symptoms post TBI. These findings are supported by several published clinical and preclinical studies showing increased inflammatory responses in patients with neuropsychiatric disorders as well as in animal models of neuropsychiatric disorders. Moreover, genome-wide association studies have provided evidence on the association between immune-related genes and neuropsychiatric disorders. Recent advances have shown the effects of inflammation on children’s neurodevelopment as seen in ASD and DCD and several other childhood neurological conditions. Moreover, inflammation is also suggested to affect the fetal brain. There is emerging evidence that inflammation and infection are responsible for preterm birth and are linked to brain injury in preterm infants. During birth, the fetal gut is colonized by maternal microbiota, directing immune system development and homeostasis. Therefore, it is reasonable to infer that any changes in the gut microbiome would impact the development of the fetal brain possibly through dysregulation of the immune responses. This is not unexpected as the gut microbiome profoundly affects neurodevelopment, immune function, and host behavioral function in mice and humans. Therefore, understanding how the gut–brain axis influences the inflammatory response under disease conditions may uncover novel insights into disease pathophysiology and yield novel therapeutic targets for neuropsychiatric disorders. Interestingly, small molecules or therapies that target inflammation have been proposed for treating neuropsychiatric disorders. These findings provide proof-of-concept evidence that aberrant inflammation can render the brain more vulnerable to neuropsychiatric/neurodevelopmental conditions and that targeting inflammation-based mechanisms may hold therapeutic promise against neuropsychiatric/neurodevelopmental conditions. Unfortunately, despite decades of efforts, the exact mechanisms by which inflammatory responses contribute to neuropsychiatric disorders remain obscure. Therefore, a better understanding of the mechanisms underlying inflammation in neuropsychiatric disorders will identify novel targets and provide opportunities for the development of novel treatments. This Special Issue aims to highlight the global research efforts aimed at exploring the mechanistic role of inflammation in neuropsychiatric disorders, identifying disease biomarkers and strategies/therapies that can attenuate the disease symptoms, and reduce the social and economic impact of neuropsychiatric disorders. For this Special Issue, we invite articles addressing findings on novel mechanisms involving neuroinflammatory responses and immune responses in neuropsychiatric disorders or neurodegenerative diseases in children, adults, and older adults. We also hope to attract studies aimed at discovering disease biomarkers for early diagnosis and novel therapeutic approaches or strategies to prevent or delay the progression of neuropsychiatric/neurodegenerative/neurodevelopmental disorders.

Dr. Mohammad Moshahid Khan
Guest Editor

Manuscript Submission Information

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  • inflammation
  • immune response
  • neurodegeneration
  • childhood neurodevelopmental disorders
  • gut-brain axis
  • behavioral functions
  • neuropsychiatric symptoms

Published Papers (1 paper)

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15 pages, 1904 KiB  
An Overview of UBTF Neuroregression Syndrome
by Anneliesse A. Braden, Jianfeng Xiao, Roderick Hori, Chester Brown and Mohammad Moshahid Khan
Brain Sci. 2024, 14(2), 179; - 15 Feb 2024
Viewed by 1498
Recently, a recurrent de novo dominant mutation in UBTF (c.628G>A, p.Glu210Lys; UBTF E210K) was identified as the cause of a neurological disorder which has been named UBTF Neuroregression Syndrome (UNS), or Childhood-Onset Neurodegeneration with Brain Atrophy (CONDBA). To date, only 17 cases have [...] Read more.
Recently, a recurrent de novo dominant mutation in UBTF (c.628G>A, p.Glu210Lys; UBTF E210K) was identified as the cause of a neurological disorder which has been named UBTF Neuroregression Syndrome (UNS), or Childhood-Onset Neurodegeneration with Brain Atrophy (CONDBA). To date, only 17 cases have been reported worldwide. The molecular etiology is a pathogenic variant, E210K, within the HMG-box 2 of Upstream Binding Transcription Factor (UBTF). UBTF, a nucleolar protein, plays an important role in ribosomal RNA (rRNA) synthesis, nucleolar integrity, and cell survival. This variant causes unstable preinitiation complexes to form, resulting in altered rDNA chromatin structures, rRNA dysregulation, DNA damage, and ultimately, neurodegeneration. Defining clinical characteristics of the disorder include but are not limited to developmental regression beginning at approximately three years of age, progressive motor dysfunction, declining cognition, ambulatory loss, and behavioral problems. Histological and neuroimaging abnormalities include cortical atrophy, white matter deficits, and enlarged ventricles. Herein, we present a detailed overview of all published cases as well as the functional roles of UBTF to better understand the pathophysiology. Bringing undiagnosed cases to the attention of clinicians and researchers by making them aware of the clinical features will improve research and support the development of therapeutic interventions. Full article
(This article belongs to the Special Issue Neuroinflammation in Neuropsychiatric Disorders)
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