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Sakurai, R.

Publications and source records attributed to Sakurai, R..

2 recordsLinked to original sources

Multimodal EEG-fNIRS Fusion for Passive BCI-based Depressive State Classification

Traditional psychiatric assessments for depression are often hindered by subjective bias and patient recall in-accuracy. This paper presents a multimodal passive Brain-Computer Interface (pBCI) designed for the objective screening of depressive traits through the end-to-end decoding of neural dynamics. We implemented a hybrid EEG-fNIRS framework to capture synchronized electro-hemodynamic responses during an emotional working memory (EWM) task. To classify sub-clinical depressive tendencies based on BDI-II scores, we utilized SincShallowNet, a deep learning architecture optimized for raw signal processing via learnable Sinc-filters. Our results demonstrate that the pBCI achieves peak performance in the auditory modality, with the integration of EEG and low-pass filtered fNIRS (0.15 Hz) yielding a balanced accuracy of 90.9% and an F1-score of 0.867. By isolating purely endogenous neural markers during the EWM maintenance phase, the system provides a robust "silent observer" for mental state monitoring. These findings validate the potential of multimodal pBCIs as high-precision, data-driven tools for early-stage depression screening, offering a scalable alternative to traditional clinical interviews and a foundation for longitudinal mental health monitoring.

neuroscience↗

Clustering by phenotype and genome-wide association study in autism

BackgroundAutism spectrum disorder (ASD) has phenotypically and genetically heterogeneous characteristics. A simulation study demonstrated that attempts to categorize patients with a complex disease into more homogeneous subgroups could have more power to elucidate hidden heritability. MethodsWe conducted cluster analyses using the k-means algorithm with a cluster number of 15 based on phenotypic variables from the Simons Simplex Collection (SSC). As a preliminary study, we conducted a conventional genome-wide association study (GWAS) with a dataset of 597 ASD cases and 370 controls. In the second step, we divided cases based on the clustering results and conducted GWAS in each of the subgroups vs controls (cluster-based GWAS). We also conducted cluster-based GWAS on another SSC dataset of 712 probands and 354 controls in the replication stage. ResultsIn the preliminary study, we observed no significant associations. In the second step of cluster-based GWASs, we identified 65 chromosomal loci, which included 30 intragenic loci located in 21 genes and 35 intergenic loci that satisfied the threshold of P<5.0x10-8. Some of these loci were located within or near previously reported candidate genes for ASD: CDH5, CNTN5, CNTNAP5, DNAH17, DPP10, DSCAM, FOXK1, GABBR2, GRIN2A5, ITPR1, NTM, SDK1, SNCA and SRRM4. Of these 65 significant chromosomal loci, rs11064685 located within the SRRM4 gene had a significantly different distribution in the cases vs. controls in the replication cohort. ConclusionsThese findings suggest that clustering may successfully identify subgroups with relatively homogeneous disease etiologies. Further cluster validation and replication studies are warranted in larger cohorts.

neuroscience↗