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Kitani, A.

Publications and source records attributed to Kitani, A..

2 recordsLinked to original sources

Predicting Alzheimer's Cognitive Resilience Score: A Comparative Study of Machine Learning Models Using RNA-seq Data

BackgroundCognitive resilience (CR) in Alzheimers disease (AD) refers to preserved cognitive function despite substantial AD pathology. Diverse biological processes have been implicated in CR, including synaptic maintenance, neuroimmune regulation, and metabolic homeostasis. However, how these mechanisms are organized into molecularly distinct CR subtypes and relate to clinical and neuroanatomical heterogeneity remains unclear. Here, we applied a machine learning framework to multi-cohort transcriptomic, proteomic, and neuroimaging data to investigate molecular subtypes of CR in AD. MethodsRNA-seq data from the Religious Orders Study and Memory and Aging Project (ROSMAP) cohort were used to train machine learning models classifying individuals with AD pathology as CR or non-CR based on residual-based resilience scores. Model development and performance estimation used nested cross-validation to minimize information leakage. Final ROSMAP-trained models were evaluated in the independent Mount Sinai Brain Bank (MSBB) cohort. Model-derived genes were used for biological interpretation and hierarchical clustering of CR individuals. The subtype structure was further evaluated in the Alzheimers Disease Neuroimaging Initiative (ADNI) cohort using cerebrospinal fluid proteomics, MRI-derived brain measures, and longitudinal MMSE data. ResultsMachine learning models showed modest but consistent predictive performance in ROSMAP, with out-of-fold AUROC values of 0.644-0.688. In the independent MSBB full cohort, AUROC values were 0.586-0.659, with improved discrimination in a top/bottom quartile analysis. Hierarchical clustering identified two major molecular subgroups among CR individuals in ROSMAP/MSBB RNA-seq data. A reduced 22-gene/protein signature showed a partial, cluster-like resemblance to this structure in ADNI cerebrospinal fluid proteomics. In ADNI, both projected CR subtypes showed preserved brain tissue-volume profiles and slower longitudinal MMSE decline compared with non-CR participants, whereas clear differences between CR subtypes were not observed. Differential CSF proteomic analysis suggested partially distinct molecular characteristics. ConclusionsThese findings suggest that CR in AD may encompass molecularly heterogeneous, subtype-like profiles that converge on broadly preserved brain structure and slower cognitive decline. Our results provide a candidate framework for stratifying resilience-associated molecular phenotypes in AD and warrant prospective and experimental validation. We also developed the Resilience Gene Analyzer, a web-based platform for visualizing gene-level contributions to CR prediction (https://igcore.cloud/GerOmics/REsilienceGeneAnalyzer/).

bioinformatics↗

GPNMB+ microglia moderate the amyloid beta-tau interaction in early Alzheimer's disease

BackgroundAlthough interactions between amyloid-beta and tau proteins have been implicated in Alzheimers disease (AD), the precise mechanisms by which these interactions contribute to disease progression are not yet fully understood. Moreover, despite the growing application of deep learning in various biomedical fields, its application in integrating networks to analyze disease mechanisms in AD research remains limited. In this study, we employed BIONIC, a deep learning-based network integration method, to integrate proteomics and protein-protein interaction data, with an aim to uncover factors that moderate the effects of the A{beta}-tau interaction on mild cognitive impairment (MCI) and early-stage AD. MethodsProteomic data from the ROSMAP cohort were integrated with protein-protein interaction (PPI) data using a Deep Learning-based model. Linear regression analysis was applied to histopathological and gene expression data, and mutual information was used to detect moderating factors. Statistical significance was determined using the Benjamini-Hochberg correction (p < 0.05). ResultsOur results suggested that astrocytes and GPNMB+ microglia moderate the A{beta}-tau interaction. Based on linear regression with histopathological and gene expression data, GFAP and IBA1 levels and GPNMB gene expression positively contributed to the interaction of tau with A{beta} in non-dementia cases, replicating the results of the network analysis. ConclusionsThese findings indicate that GPNMB+ microglia moderate the A{beta}-tau interaction in early AD and therefore are a novel therapeutic target. To facilitate further research, we have made the integrated network available as a visualization tool for the scientific community (URL: https://igcore.cloud/GerOmics/AlzPPMap).

systems biology↗