Aicardi syndrome is a congenital neurodevelopmental disorder associated with significant cognitive and motor impairment. Diffusion tensor imaging was performed on two subjects with Aicardi syndrome, as well as on two matched subjects with callosal agenesis and cortical malformations but not a clinical diagnosis of Aicardi syndrome. Whole-brain three-dimensional fiber tractography was performed, and major white matter tracts were isolated using standard tracking protocols. One Aicardi subject demonstrated an almost complete lack of normal corticocortical connectivity, with only the left inferior fronto-occipital fasciculus recovered by diffusion tensor tractography. A second Aicardi subject exhibited evidence of bilateral cingulum bundles and left uncinate fasciculus, but other corticocortical tracts were not recovered. Major subcortical white matter tracts, including corticospinal, pontocerebellar, and anterior thalamic radiation tracts, were recovered in both Aicardi subjects. In contrast, diffusion tensor tractography analysis on the two matched control subjects with callosal agenesis and cortical malformations recovered all major intrahemispheric cortical and subcortical white matter tracts. These findings reveal a widespread disruption in the corticocortical white matter organization of individuals with Aicardi syndrome. Furthermore, such disruption in white matter organization appears to be a feature specific to Aicardi syndrome, and not shared by other neurodevelopmental disorders with similar anatomic manifestations.
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http://dx.doi.org/10.1016/j.pediatrneurol.2010.03.005 | DOI Listing |
Pediatr Rheumatol Online J
January 2025
Laboratory of Autoimmunity and Inflammation, Center for Clinical, Biomedical Research Foundation, Experimental Surgery and Translational Research, Academy of Athens, Athens, Greece.
Background: Type I interferonopathies including Aicardi-Goutiéres Syndrome (AGS) represent a heterogeneous group of clinical phenotypes. Herein, we present a Case with combined AGS and Cornelia de Lange Syndrome (CdLS)-a cohesinopathy-with comprehensive analysis of the immune and genomic abnormalities.
Case And Methods: A 20-year old man presented with chilblain lesions and resorption of distal phalanges of fingers and toes, somatic and psychomotor retardation, microcephaly, synophrys, hearing losing and other aberrancies consistent with the phenotype of CdLS.
Methods Enzymol
January 2025
St.Vincent's Institute of Medical Research, Fitzroy, Victoria, Australia; Department of Medicine, St. Vincent's Hospital, Melbourne Medical School, University of Melbourne, Fitzroy, Victoria, Australia; Centre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Research, Clayton, Victoria, Australia; Department of Molecular and Translational Science, Monash University, Clayton, Victoria, Australia. Electronic address:
Adenosine-to-inosine (A-to-I) editing, is a highly prevalent posttranscriptional modification of RNA, mediated by the adenosine deaminases acting on RNA (ADAR) proteins. Mammalian transcriptomes contain tens of thousands to millions of A-to-I editing events. Mutations in ADAR can result in rare autoinflammatory disorders such as Aicardi-Goutières syndrome (AGS) through to irreversible conditions such as motor neuron disease, amyotrophic lateral sclerosis (ALS).
View Article and Find Full Text PDFFront Immunol
January 2025
Instituto Murciano de Investigación Biosanitaria (IMIB)-Pascual Parrilla, Murcia, Spain.
[This corrects the article DOI: 10.3389/fimmu.2023.
View Article and Find Full Text PDFDev Med Child Neurol
January 2025
Paediatric Neurology, University of Sydney and Children's Hospital at Westmead, Westmead, Australia.
CNS Neurosci Ther
January 2025
Jiujiang Clinical Precision Medicine Research Center, Jiujiang, Jiangxi, China.
Background: Adenosine deaminase action on RNA 1 (ADAR1) can convert the adenosine in double-stranded RNA (dsRNA) molecules into inosine in a process known as A-to-I RNA editing. ADAR1 regulates gene expression output by interacting with RNA and other proteins; plays important roles in development, including growth; and is linked to innate immunity, tumors, and central nervous system (CNS) diseases.
Results: In recent years, the role of ADAR1 in tumors has been widely discussed, but its role in CNS diseases has not been reviewed.
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