Publications by authors named "A M Kloster"

Objective: To establish an interaction network for genes related to premature ovarian insufficiency (POI) and insomnia, and to identify biological processes that connect POI to the physiological clock.

Methods: Previously reported lists of genes associated to POI and insomnia were contrasted and their intersection was used as input on protein-protein interaction analyses. POI-associated genes were contrasted with gene expression markers for neural circadian control and enriched pathways among their shared content were dissected.

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Article Synopsis
  • Neurodevelopmental disorders and sleep issues share common genetic risks, with specific variants linked to rare syndromes that report sleep disturbances.
  • The study aimed to identify biological processes affected by these genetic variants by comparing DEAF1 regulatory target genes with insomnia-associated genes.
  • Findings revealed 39 overlapping genes primarily connected to immune processes, cell cycle regulation, and protein degradation, suggesting they may play a role in insomnia among patients with these genetic mutations.*
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Article Synopsis
  • - The study investigates sleep disturbances and epilepsy in patients with SYNGAP1-associated syndrome, a rare neurodevelopmental disorder that leads to intellectual disability and other challenges.
  • - An online survey involving 11 caregivers revealed that 82% of patients experienced epilepsy, with a significant number showing drug-resistant seizures and poor sleep habits, as assessed by standardized questionnaires.
  • - Findings indicate that both patients and caregivers struggle with sleep quality, underscoring the need for further research and interventions aimed at improving sleep and overall quality of life in individuals affected by this syndrome.
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Pogo transposable element-derived protein with ZNF domain () gene encodes a chromatin regulator and rare variants on this gene have been associated with a broad spectrum of neurodevelopmental disorders, such as White-Sutton syndrome. Patient clinical manifestations frequently include developmental delay, autism spectrum disorder and obesity. Sleep disturbances are also commonly observed in these patients, yet the biological pathways which link sleep traits to the -associated syndrome remain unclear.

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