{"doi":"10.1111/cns.14558","title":"Sleep and\n                    <scp>APOE</scp>\n                    ‐ε4 have a synergistic effect on plasma biomarkers and longitudinal cognitive decline in older adults","abstract":"<jats:title>Abstract</jats:title>\n                  <jats:sec>\n                    <jats:title>Background</jats:title>\n                    <jats:p>Sleep disorders are prevalent among patients with Alzheimer's disease (AD), and the APOE ε4 genotype is a key genetic risk factor for sporadic AD. However, the combined effect of the genotype and sleep disorders on cognitive decline remains uncertain.</jats:p>\n                  </jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods</jats:title>\n                    <jats:p>A total of 972 participants were drawn from the SILCODE cohort, comprising 655 without the ε4 allele (APOE−) and 317 with ε4 allele (APOE+). Data were collected, including neuropsychological assessments, sleep measurements, plasma biomarkers, and PET imaging. A Sleep Composite Index (SCI) was created, categorizing participants into high risk (Sleep+) and low risk (Sleep−).</jats:p>\n                  </jats:sec>\n                  <jats:sec>\n                    <jats:title>Results</jats:title>\n                    <jats:p>Significant predictions of dementia risk associated with plasma p‐tau181, neurofilament light chain (NfL), and SCI. Individuals with both Sleep+ and APOE+ had a higher risk of dementia compared to those with Sleep‐. The Sleep+/APOE+ group had higher plasma NfL levels than the Sleep−/APOE− group. Similar trends emerged in plasma NfL levels among the Aβ PET‐positive subgroup. Plasma NfL levels explained 23% of the relationship between SCI and cognitive impairment.</jats:p>\n                  </jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion</jats:title>\n                    <jats:p>Our study highlights sleep disorder was associated with cognitive decline, with plasma NfL playing a partial mediating role. These findings explain how sleep disorders affect cognitive function and emphasize the importance of healthy sleep for older adults.</jats:p>\n                  </jats:sec>","journal":"CNS Neuroscience &amp; Therapeutics","year":2024,"id":637236,"datarank":0.38474240361923057,"base_score":2.5649493574615367,"endowment":2.5649493574615367,"self_citation_contribution":0.38474240361923057,"citation_network_contribution":0.0,"self_endowment_contribution":0.38474240361923057,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":12,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":null,"is_data_producer":false,"deposit_databanks":null,"is_oa":false,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":null,"fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":478691,"name":"Xia Zhou","orcid":"0009-0008-6364-1530","position":1,"is_corresponding":false},{"id":1383264,"name":"Zhengbo He","orcid":null,"position":2,"is_corresponding":false},{"id":1654448,"name":"Beiqi He","orcid":null,"position":3,"is_corresponding":false},{"id":1057304,"name":"Ke Wan","orcid":"0000-0002-1563-7181","position":4,"is_corresponding":false},{"id":27368,"name":"Min Wei","orcid":"0000-0002-7015-334X","position":5,"is_corresponding":false},{"id":277015,"name":"Tengfei Guo","orcid":"0000-0003-2982-0865","position":6,"is_corresponding":false},{"id":267079,"name":"Ying Han","orcid":"0000-0003-0377-7424","position":7,"is_corresponding":false},{"id":1374675,"name":"Xianfeng Yu","orcid":"0000-0003-0589-2178","position":0,"is_corresponding":false}],"reference_count":0,"raw_metadata":{"has_enrichment":true,"resolved":true,"title":"Sleep and\n                    <scp>APOE</scp>\n                    ‐ε4 have a synergistic effect on plasma biomarkers and longitudinal cognitive decline in older adults","abstract":"<jats:title>Abstract</jats:title>\n                  <jats:sec>\n                    <jats:title>Background</jats:title>\n                    <jats:p>Sleep disorders are prevalent among patients with Alzheimer's disease (AD), and the APOE ε4 genotype is a key genetic risk factor for sporadic AD. However, the combined effect of the genotype and sleep disorders on cognitive decline remains uncertain.</jats:p>\n                  </jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods</jats:title>\n                    <jats:p>A total of 972 participants were drawn from the SILCODE cohort, comprising 655 without the ε4 allele (APOE−) and 317 with ε4 allele (APOE+). Data were collected, including neuropsychological assessments, sleep measurements, plasma biomarkers, and PET imaging. A Sleep Composite Index (SCI) was created, categorizing participants into high risk (Sleep+) and low risk (Sleep−).</jats:p>\n                  </jats:sec>\n                  <jats:sec>\n                    <jats:title>Results</jats:title>\n                    <jats:p>Significant predictions of dementia risk associated with plasma p‐tau181, neurofilament light chain (NfL), and SCI. Individuals with both Sleep+ and APOE+ had a higher risk of dementia compared to those with Sleep‐. The Sleep+/APOE+ group had higher plasma NfL levels than the Sleep−/APOE− group. Similar trends emerged in plasma NfL levels among the Aβ PET‐positive subgroup. Plasma NfL levels explained 23% of the relationship between SCI and cognitive impairment.</jats:p>\n                  </jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion</jats:title>\n                    <jats:p>Our study highlights sleep disorder was associated with cognitive decline, with plasma NfL playing a partial mediating role. These findings explain how sleep disorders affect cognitive function and emphasize the importance of healthy sleep for older adults.</jats:p>\n                  </jats:sec>","is_dataset_classified":null,"base_score":2.4849066497880004,"endowment":2.4849066497880004,"datacite_reuse_total":0,"file_count":0,"downloads":0,"views":0,"has_version_chain":false,"is_dataset":false,"is_oa":false,"pmid":"38421124","pmcid":"PMC10850800","openalex_id":"https://openalex.org/W4391635419","authors":[],"funders":[{"funder_name":"National Natural Science Foundation of China","grant_id":"61633018","title":null},{"funder_name":"National Natural Science Foundation of China","grant_id":"82020108013","title":null},{"funder_name":"National Natural Science Foundation of China","grant_id":"82171197","title":null},{"funder_name":"Guangdong Basic and Applied Basic Science Foundation for Distinguished Young Scholars","grant_id":"2023B1515020113","title":null}],"total_grants":4,"fwci":2.6034,"citation_percentile":0.89280834,"influential_citations":0,"citation_trend":[{"year":2024,"count":2},{"year":2025,"count":6},{"year":2026,"count":3}],"oa_status":"gold","license":"cc-by","oa_locations":[{"url":"https://onlinelibrary.wiley.com/doi/pdfdirect/10.1111/cns.14558","host_type":"journal"},{"url":"https://onlinelibrary.wiley.com/doi/pdfdirect/10.1111/cns.14558","host_type":"publisher"},{"url":"https://onlinelibrary.wiley.com/doi/pdf/10.1111/cns.14558","host_type":"publisher"},{"url":"https://onlinelibrary.wiley.com/doi/full-xml/10.1111/cns.14558","host_type":"publisher"},{"url":"https://doi.org/10.1111/cns.14558","host_type":"journal"},{"url":"https://pubmed.ncbi.nlm.nih.gov/38421124","host_type":"repository"},{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/10850800","host_type":"repository"},{"url":"https://pmc.ncbi.nlm.nih.gov/articles/PMC10850800/pdf/CNS-30-e14558.pdf","host_type":"repository"},{"url":"https://europepmc.org/articles/PMC10850800","host_type":"Europe_PMC"},{"url":"https://europepmc.org/articles/PMC10850800?pdf=render","host_type":"Europe_PMC"}],"fields_of_study":["Sleep and Wakefulness Research","Sleep and related disorders","Circadian rhythm and melatonin"],"mesh_terms":["Aged","Alzheimer Disease","Humans","Sleep","Sleep Wake Disorders","Biomarkers","Amyloid beta-Peptides","tau Proteins","Apolipoprotein E4","Cognitive Dysfunction"],"keywords":["Apolipoprotein E","Sleep (system call)","Cognitive decline","Genotype","Medicine","Cognition","Disease","Cognitive impairment","Oncology","Psychiatry","Internal medicine","Clinical psychology","Psychology","Gerontology","Dementia","Biology","Genetics","Gene","Sleep","Alzheimer's disease","Discrimination","Biomarkers","Apoe Ε4"],"sdg_mappings":[{"sdg_number":0,"sdg_label":"Good health and well-being"}],"linked_datasets":[],"clinical_trials":[],"software_tools":[],"database_accessions":[{"name":"refsnp"},{"name":"nct"}],"source":"live","citation_network_status":"fetched"},"created_at":"2026-08-06T18:36:30.195074Z","pmid":null,"pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}