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From Molecular Mechanism to Therapy in Autism Spectrum Disorder: 2nd Edition

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (20 November 2024) | Viewed by 2234

Special Issue Editors

Prof. Dr. Lucia Margari

E-Mail Website
Guest Editor
Child and Adolescent Neuropsychiatry Unit, University of Bari “Aldo Moro”, 70124 Bari, Italy
Interests: neurodevelopmental disorders; autism spectrum disorder; child and adolescent neuropsychiatry; psychopathology; mental illness; psychopharmacology
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Emilia Matera

E-Mail Website
Guest Editor
Child and Adolescent Neuropsychiatry Unit, University of Bari “Aldo Moro”, 70124 Bari, Italy
Interests: autism spectrum disorder; neurodevelopmental disorders; molecular mechanisms; targeted treatments; psychopathology; clinical psychiatry; psychopharmacology; psychoneuroendocrinology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

On behalf of the editorial team of the International Journal of Molecular Sciences (IJMS), we are pleased to announce the launch of a new Special Issue, entitled "From Molecular Mechanisms and Therapy in Autism Spectrum Disorders (ASD)", lead by Prof. Dr. Lucia Margari and Prof. Dr. Emilia Matera and assisted by the Promotion Editors Dr. Alessandra Gabellone and Dr. Lucia Marzulli (University of Bari “Aldo Moro”).

ASD is a complex neurodevelopmental disorder with a strong genetic basis, characterized by a great heterogeneity in its phenotypic features (onset, symptoms, comorbidities, adaptive behaviors, cognitive abilities, and developmental trajectories), etiological factors (genetic, immunological, and environmental), disease course, and response to treatment.

A major challenge is to advance the results of discovering the neurobiological mechanisms underlying ASD and then translating this knowledge into a mechanism-based, combined, and effective treatment design targeting multiple molecules and pathways, including drug medications, habilitation and educational approaches, and the use of new technologies.

Researchers and authors are invited to submit original research and literature reviews that may have a significant impact on genetics, neuroimaging, clinical presentation, diagnostic tools, and novel therapeutic as well as intervention approaches in ASD.

Prof. Dr. Lucia Margari
Prof. Dr. Emilia Matera
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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 disorder
  • neurobiological mechanisms
  • molecular mechanisms
  • neuroimmune
  • pathogenesis
  • treatment
  • management

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Related Special Issue

Published Papers (2 papers)

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Research

16 pages, 1334 KiB  
Article
Association between Autism Spectrum Disorder, Trace Elements, and Intracranial Fluid Spaces
by Matej Mlinarič, Maja Jekovec Vrhovšek, David Neubauer, Alenka France Štiglic and Joško Osredkar
Int. J. Mol. Sci. 2024, 25(15), 8050; https://doi.org/10.3390/ijms25158050 - 24 Jul 2024
Viewed by 915
Abstract
(1) Autism spectrum disorder (ASD) belongs to the group of complex developmental disorders. Novel studies have suggested that genetic and environmental factors equally affect the risk of ASD. Identification of environmental factors involved in the development of ASD is therefore crucial for a [...] Read more.
(1) Autism spectrum disorder (ASD) belongs to the group of complex developmental disorders. Novel studies have suggested that genetic and environmental factors equally affect the risk of ASD. Identification of environmental factors involved in the development of ASD is therefore crucial for a better understanding of its etiology. Whether there is a causal link between trace elements, brain magnetic resonance imaging (MRI), and ASD remains a matter of debate and requires further studies. (2) In the prospective part of the study, we included 194 children, including an age-matched control group; in the retrospective study, 28 children with available MRI imaging were included. All children had urine analysis of trace elements performed. In those with available brain MRI, linear indexes for the ventricular volumes were measured and calculated. (3) We found the highest vanadium, rubidium, thallium, and silver levels in children with ASD. These elements also correlated with the estimated ventricular volume based on MRI indexes in children with ASD in the subanalysis. However, the severity of the deficits did not correlate with brain MRI indexes of our elements, except negatively with magnesium. (4) Trace elements have an impact on children with ASD, but further multi-centric studies are needed to explain the pathophysiological mechanisms. Full article
(This article belongs to the Special Issue From Molecular Mechanism to Therapy in Autism Spectrum Disorder: 2nd Edition)
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16 pages, 3996 KiB  
Article
Adult Inception of Ketogenic Diet Therapy Increases Sleep during the Dark Cycle in C57BL/6J Wild Type and Fragile X Mice
by Pamela R. Westmark, Timothy J. Swietlik, Ethan Runde, Brian Corsiga, Rachel Nissan, Brynne Boeck, Ricky Granger, Erica Jennings, Maya Nebbia, Andrew Thauwald, Greg Lyon, Rama K. Maganti and Cara J. Westmark
Int. J. Mol. Sci. 2024, 25(12), 6679; https://doi.org/10.3390/ijms25126679 - 18 Jun 2024
Cited by 1 | Viewed by 862
Abstract
Sleep problems are a significant phenotype in children with fragile X syndrome. Our prior work assessed sleep–wake cycles in Fmr1KO male mice and wild type (WT) littermate controls in response to ketogenic diet therapy where mice were treated from weaning (postnatal day [...] Read more.
Sleep problems are a significant phenotype in children with fragile X syndrome. Our prior work assessed sleep–wake cycles in Fmr1KO male mice and wild type (WT) littermate controls in response to ketogenic diet therapy where mice were treated from weaning (postnatal day 18) through study completion (5–6 months of age). A potentially confounding issue with commencing treatment during an active period of growth is the significant reduction in weight gain in response to the ketogenic diet. The aim here was to employ sleep electroencephalography (EEG) to assess sleep–wake cycles in mice in response to the Fmr1 genotype and a ketogenic diet, with treatment starting at postnatal day 95. EEG results were compared with prior sleep outcomes to determine if the later intervention was efficacious, as well as with published rest-activity patterns to determine if actigraphy is a viable surrogate for sleep EEG. The data replicated findings that Fmr1KO mice exhibit sleep–wake patterns similar to wild type littermates during the dark cycle when maintained on a control purified-ingredient diet but revealed a genotype-specific difference during hours 4–6 of the light cycle of the increased wake (decreased sleep and NREM) state in Fmr1KO mice. Treatment with a high-fat, low-carbohydrate ketogenic diet increased the percentage of NREM sleep in both wild type and Fmr1KO mice during the dark cycle. Differences in sleep microstructure (length of wake bouts) supported the altered sleep states in response to ketogenic diet. Commencing ketogenic diet treatment in adulthood resulted in a 15% (WT) and 8.6% (Fmr1KO) decrease in body weight after 28 days of treatment, but not the severe reduction in body weight associated with starting treatment at weaning. We conclude that the lack of evidence for improved sleep during the light cycle (mouse sleep time) in Fmr1KO mice in response to ketogenic diet therapy in two studies suggests that ketogenic diet may not be beneficial in treating sleep problems associated with fragile X and that actigraphy is not a reliable surrogate for sleep EEG in mice. Full article
(This article belongs to the Special Issue From Molecular Mechanism to Therapy in Autism Spectrum Disorder: 2nd Edition)
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