| Institution: | 1. George S. Wise Faculty of Life Sciences, Tel Aviv University, Tel Aviv, Israel;2. The Behavioral Neurogenetics Center, The Edmond and Lily Safra Children's Hospital, Sheba Medical Center, Ramat Gan, Israel;3. https://orcid.org/0000-0002-5334-2851;4. Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel;5. Ehud Mekori‐Domachevsky, The Child Psychiatry Division, Edmond and Lily Safra Children's Hospital, Sheba Medical Center, 52621 Tel Hashomer, Israel.;6. Sagol School of Neuroscience, Tel Aviv University, Tel Aviv, Israel;7. Biological Psychiatry Laboratory, Felsenstein Medical Research Center, Petah Tikva, Israel |
| Abstract: | 22q11.2 deletion syndrome (22q11.DS) is a neurogenetic disorder caused by a microdeletion in chromosome 22. Its phenotype includes high rates of psychiatric disorders, immune system abnormalities, and cognitive impairments. We assessed the quality of sleep in 22q11.2DS and its potential link to inflammatory markers and cognitive deficits. Thirty‐three 22q11.2DS individuals and 24 healthy controls were studied. Sleep parameters were assessed by the Pittsburgh sleep quality index (PSQI) questionnaire and correlated with serum cytokine levels and cognitive functioning, measured using the Penn computerized neurocognitive battery (CNB). The 22q11.2DS individuals had significantly worse sleep quality scores than the controls, unrelated to the psychiatric or physical comorbidities common to 22q11.2DS. Interleukin 6 levels were correlated with the overall score of the PSQI questionnaire for nonpsychotic 22q11.2DS participants only. Several domains of the CNB were associated with poorer sleep quality, suggesting that cognitive impairments in 22q11.2DS may be at least partially explained by poor sleep quality. Our findings confirm sleep impairments in individuals with 22q11.2DS, which might negatively affect their cognitive functioning, and corroborate a potential role of immunological pathways in the 22q11.2DS neuro‐phenotype. |
