Dietary index for gut microbiota score is inversely associated with carotid calcified plaque score in ischemic stroke patients.

Sleep difficulties are among the most common clinical manifestations in neurodevelopmental disorders (NDDs) (). Prevalence of sleep problems is higher in individuals with NDDs than in neurotypicals, with estimates of 50–95% in NDD populations compared to 25% in neurotypical populations (). Although the range of prevalence estimates in NDDs may be explained by methodological factors, frequency and other features of different sleep problems seem to be disorder-specific (, ). For example, in their meta-analysis of 19 genetic NDDs, Agar and colleagues reported that prevalence of sleep-related breathing difficulties ranged from 2% in Angelman syndrome (AS) and Jacobsen syndrome to over 70% in mucopolysaccharidoses while excessive daytime sleepiness ranged from 9% in Jacobsen syndrome to 60% in Smith–Magenis syndrome (). Considering that sleep problems are associated with poorer cognitive and behavioral outcomes in the general population and NDDs (, , ), characterizing the most common types of sleep difficulties in a particular disorder may lead to their earlier identification and to more targeted treatments (, ). Underscoring the importance of delineating sleep difficulties in NDDs, a recently organized a workshop on Neurodevelopmental Disorders and Sleep was by the National Heart, Lung, and Blood Institute (NHLBI) at the National Institutes of Health (NIH) to identify research gaps and opportunities in the field. The conclusions of the event included limited availability of mechanistic data and use of objective diagnostic methods. They also highlighted the correlation between sleep disturbances and more severe NDD symptoms (National Heart, Lung, and Blood Institute (NHLBI)/National Institutes of Health (NIH) Neurodevelopmental Disorders and Sleep Workshop (May 15–16, 2025): ). A NIH-funded Rare Diseases Clinical Research Network (RDCRN) project on three severe NDDs linked by epigenetic mechanisms, Angelman syndrome (AS), Prader-Willi syndrome (PWS), and Rett syndrome (RTT), has recently characterized sleep disturbances in a large sample of affected individuals (), the findings have implications for severe NDDs in general. AS is a rare genetic disorder affecting both sexes and with a prevalence of 1 in 12,000–24,000 (, ). It is associated with a loss in the ubiquitin protein ligand E3A (UBE3A), key for protein homeostasis, due most commonly to a deletion of the maternal chromosome 15q11-q13 region containing the maternally imprinted gene (only the maternal copy is active in neurons) (). AS is characterized by severe global developmental delay/severe intellectual disability, absent or minimal spoken language, seizures, happy demeanor and outbursts of laughter, gross and fine motor deficits, tremors, hyperactivity, stereotypical behavior, anxiety, gastrointestinal problems, and sleep disturbances (, ). PWS affects both males and females, with overall prevalence estimates of 1 in 10,000–30,000 births (). It is associated, in most cases, with a loss due to a deletion of the paternally imprinted chromosome 15q11-q13 region. In contrast to AS, PWS is not linked to the loss of function of but of other genes in the region (e.g., ) (, , ). PWS’ phenotype is characterized earlier by developmental delay/mild–moderate intellectual disability, hypotonia, and feeding difficulties, which is followed in childhood by hyperphagia that is frequently associated with early-onset morbid obesity, and sleep-disordered breathing (, , , , ). RTT occurs predominantly in females, with a prevalence of 1 in 10,000–23,000 (), with most cases linked to loss-of-function variants in the X-linked gene that encodes the transcriptional regulator methyl-CpG-binding protein 2 () (). RTT is characterized by developmental regression following an initial period of apparently typical development. Loss of spoken language and purposeful hand use, stereotypical hand movements, and impaired ambulation constitute RTT’s core diagnostic features (, ). The regression phase is followed by a period of relative stabilization when severe cognitive impairment and other clinical manifestations become evident, including seizures, growth failure, gastroesophageal symptoms (e.g., constipation), scoliosis, breathing and autonomic dysfunction, behavioral abnormalities, and sleep problems (). Although broadly linked by epigenetic mechanisms, each of the aforementioned NDDs involves different genes and signaling pathways. Therefore, it is not surprising that they present with different clinical manifestations including disorder-specific sleep abnormalities. In AS, sleep disturbances such as difficulties initiating and maintaining sleep, sleep terrors, sleep-related seizures, disorientation when aroused, snoring, teeth grinding, bed wetting, sleepwalking, and circadian rhythm abnormalities have been reported (, , , ). Studies from AS mouse models have shown mixed results; one found that circadian rhythms were intact, but abnormal sleep patterns arose from a deficit in accu