BackgroundObstructive sleep apnea （OSA） represents a potential modifiable risk factor for cognitive impairment， while spatial navigation performance serves as a sensitive marker to detect such deficits at an early stage. Currently， polysomnography （PSG） is the gold standard for OSA diagnosis， with the apnea hypopnea index （AHI） used to stratify the disease severity. Nevertheless， AHI alone cannot fully explain the individual variability in cognitive impairment among OSA patients. Existing evidence indicates that sleep architecture disruption impairs spatial memory consolidation and subsequently alters spatial navigation through pathways independent of AHI， yet this hypothesis remains unvalidated in routine clinical OSA cohorts. ObjectiveTo compare the global cognitive function and spatial navigation performance across OSA patients of varying severities， and to analyze associated factors of spatial navigation performance， so as to provide clinical evidence for the early identification and intervention of cognitive impairment in OSA patients. MethodsThis cross-sectional study consecutively enrolled 135 outpatients from the Mental Health Center of Inner Mongolia Autonomous Region from March 8， 2024 to September 12， 2025. All participants completed PSG monitoring and fulfilled the OSA diagnostic criteria outlined in the Guidelines for the Diagnosis and Treatment of Adult Obstructive Sleep Apnea. Subjects were stratified into mild （5 ≤AHI < 15 events/h）， moderate （15 ≤ AHI < 30 events/h）， and severe （AHI ≥ 30 events/h） groups based on AHI values， and all PSG sleep architecture parameters were extracted for statistical analysis. Global cognitive function was evaluated using the Mini-Mental State Examination （MMSE）， the Trail Making Test （including TMT-A and TMT-B）， and two subtasks from the THINC Integrated Toolkit （THINC-it）： the Spotter test （choice reaction time， CRT） and the Codebreaker test （digit symbol substitution test， DSST）. Spatial navigation performance was assessed through the Santa Barbara Sense of Direction Scale （SBSOD） and the computerized AMUNET spatial navigation test. ResultsAmong the 135 OSA patients， 46 （34.07%） were classified into the mild group， 47 （34.82%） into the moderate group， and 42 （31.11%） into the severe group. In terms of cognitive function， there were no statistically significant intergroup differences across three groups in CRT， consecutive correct DSST responses， MMSE scores， and completion time of TMT-A and TMT-B （P>0.05）. Regarding spatial navigation performance， no statistically significant differences were observed among three groups in SBSOD scores and the outcomes of the four AMUNET subtasks （P>0.05）. Spearman correlation analyses revealed that the performance on the delayed allocentric AMUNET subtask was positively correlated with stage N2 duration， percentage of stage N2 sleep （N2%）， and rapid eye movement （REM） latency （r=0.277， 0.296， 0.239， P_FDR<0.05）. In contrast， this subtask exhibited negative correlations with REM duration， percentage of REM sleep （REM%）， stage N3 duration and percentage of stage N3 sleep （N3%） （r=-0.223–-0.175， P_FDR<0.05）. SBSOD score was positively correlated with the completion time of TMT-A and TMT-B （r=0.236， 0.278）， and negatively correlated with MMSE scores （r=-0.311）. For AMUNET indices， performance on the allocentric navigation subtask showed a positive correlation with CRT （r=0.013）. Moreover， performance of both egocentric and allocentric navigation subtasks yielded positive correlations with the completion time of TMT-A and TMT-B （r=0.191–0.265， P_FDR<0.05）. Performance on the egocentric， allocentric， and combined egocentric–allocentric navigation subtasks was negatively correlated with MMSE scores and the consecutive correct DSST responses （r=-0.318–-0.207， P_FDR<0.05）. Hierarchical multiple liner regression analysis demonstrated that after controlling for baseline characteristics and global cognitive function， N2% emerged as a positive predictor of the delayed allocentric navigation subtask performance （β=0.242， 95% CI： 0.104–1.463）. ConclusionPatients with OSA across all severity strata exhibit comparable global cognitive function and spatial navigation performance. Spatial memory is associated with sleep architecture parameters， among which N2% acts as an independent positive predictor of spatial memory performance. ［Funded by Natural Science Foundation Project of Inner Mongolia Autonomous Region （number， 2024QN08050）； Science and Technology Project for High-Level Clinical Specialty Development of Public Hospitals of the Capital Region under the Autonomous Region Health Commission of Inner Mongolia Autonomous Region in 2023 （number， 2023SGGZ047）］

The dihydrofolate reductase (dhfr) and dihydropteroate synthetase (dhps) genes of Plasmodium vivax, as antifolate resistance-associated genes were used for drug resistance surveillance. A total of 375 P. vivax isolates collected from different geographical locations in China in 2009-2019 were used to sequence Pvdhfr and Pvdhps. The majority of the isolates harbored a mutant type allele for Pvdhfr (94.5%) and Pvdhps (68.2%). The most predominant point mutations were S117T/N (77.7%) in Pvdhfr and A383G (66.8%) in Pvdhps. Amino acid changes were identified at nine residues in Pvdhfr. A quadruple-mutant haplotype at 57, 58, 61, and 117 was the most frequent (57.4%) among 16 distinct Pvdhfr haplotypes. Mutations in Pvdhps were detected at six codons, and the double-mutant A383G/A553G was the most prevalent (39.3%). Pvdhfr exhibited a higher mutation prevalence and greater diversity than Pvdhps in China. Most isolates from Yunnan carried multiple mutant haplotypes, while the majority of samples from temperate regions and Hainan Island harbored the wild type or single mutant type. This study indicated that the antifolate resistance levels of P. vivax parasites were different across China and molecular markers could be used to rapidly monitor drug resistance. Results provided evidence for updating national drug policy and treatment guidelines.
Antimalarials/pharmacology* ; China/epidemiology* ; Drug Combinations ; Drug Resistance/genetics* ; Folic Acid Antagonists/pharmacology* ; Humans ; Mutation ; Plasmodium vivax/genetics* ; Prevalence