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Cells
Special Issues
Molecular Mechanisms of Autism Spectrum Disorder
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Molecular Mechanisms of Autism Spectrum Disorder

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

Deadline for manuscript submissions: 20 October 2024 | Viewed by 1110

Special Issue Editors

Dr. Tanya Gandhi

E-Mail
Guest Editor
Department of Comparative Biomedical Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA 70806, USA
Interests: autism spectrum disorder; neurodevelopmental disorders; molecular and cellular mechanisms; neurobiological mechanisms; treatment approaches; intervention strategies; behavioral and neuroanatomical alterations
Dr. Charles Lee

E-Mail Website
Guest Editor
School of Veterinary Medicine, Baton Rouge, LA, USA
Interests: neuron; perineuronal net; synapse; membrane; glia; morphology; thalamus; cortex; inferior colliculus; auditory; sensory; neurodegeneration; neurodevelopment

Special Issue Information

Autism spectrum disorder (ASD) is a group of neurodevelopmental disorders characterized by social interaction and communication deficits, repetitive, restricted behaviors, and variable co-morbid conditions. The etiological heterogeneity of ASD encompasses complex interactions of genetic, immunological, and environmental factors that result in alterations to brain function and structure, which influence the onset of these conditions. The emergence of ASD is influenced by several molecular mechanisms that are the focus of diagnostic and intervention strategies; however, our understanding of these mechanisms remains incomplete. Such heterogeneous etiological factors contribute greatly to the development, prognosis, and variability of autistic traits.

This Special Issue aims to assemble original research and literature reviews that address the latest developments in the molecular mechanisms of autism spectrum disorder. We hope that contributions to this Special Issue will have a significant impact on ASD research in terms of understanding its molecular etiology and developing novel therapeutic strategies.

Dr. Tanya Gandhi
Dr. Charles Lee
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 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. 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

  • autism spectrum disorder
  • neurodevelopmental disorders
  • molecular mechanisms
  • cellular-molecular mechanisms
  • neurobiological mechanisms
  • neural mechanisms
  • intervention approaches
  • treatment strategies

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Published Papers (1 paper)

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Research

26 pages, 46310 KiB  
Article
iPSC-Derived Astrocytes and Neurons Replicate Brain Gene Expression, Epigenetic, Cell Morphology and Connectivity Alterations Found in Autism
by Hamid Mostafavi Abdolmaleky, Reza Alam, Shabnam Nohesara, Richard C. Deth and Jin-Rong Zhou
Cells 2024, 13(13), 1095; https://doi.org/10.3390/cells13131095 - 25 Jun 2024
Viewed by 890
Abstract
Excessive inflammatory reactions and oxidative stress are well-recognized molecular findings in autism and these processes can affect or be affected by the epigenetic landscape. Nonetheless, adequate therapeutics are unavailable, as patient-specific brain molecular markers for individualized therapies remain challenging. Methods: We used iPSC-derived [...] Read more.
Excessive inflammatory reactions and oxidative stress are well-recognized molecular findings in autism and these processes can affect or be affected by the epigenetic landscape. Nonetheless, adequate therapeutics are unavailable, as patient-specific brain molecular markers for individualized therapies remain challenging. Methods: We used iPSC-derived neurons and astrocytes of patients with autism vs. controls (5/group) to examine whether they replicate the postmortem brain expression/epigenetic alterations of autism. Additionally, DNA methylation of 10 postmortem brain samples (5/group) was analyzed for genes affected in PSC-derived cells. Results: We found hyperexpression of TGFB1, TGFB2, IL6 and IFI16 and decreased expression of HAP1, SIRT1, NURR1, RELN, GPX1, EN2, SLC1A2 and SLC1A3 in the astrocytes of patients with autism, along with DNA hypomethylation of TGFB2, IL6, TNFA and EN2 gene promoters and a decrease in HAP1 promoter 5-hydroxymethylation in the astrocytes of patients with autism. In neurons, HAP1 and IL6 expression trended alike. While HAP1 promoter was hypermethylated in neurons, IFI16 and SLC1A3 promoters were hypomethylated and TGFB2 exhibited increased promoter 5-hydroxymethlation. We also found a reduction in neuronal arborization, spine size, growth rate, and migration, but increased astrocyte size and a reduced growth rate in autism. In postmortem brain samples, we found DNA hypomethylation of TGFB2 and IFI16 promoter regions, but DNA hypermethylation of HAP1 and SLC1A2 promoters in autism. Conclusion: Autism-associated expression/epigenetic alterations in iPSC-derived cells replicated those reported in the literature, making them appropriate surrogates to study disease pathogenesis or patient-specific therapeutics. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Autism Spectrum Disorder)
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