用多平面融合+可解释注意力机制,提升阿尔茨海默病早期诊断准确率。
An Interpretable Multi-Plane Fusion Framework With Kolmogorov-Arnold Network Guided Attention Enhancement for Alzheimer's Disease Diagnosis
- 融合冠状、矢状、轴向三平面MRI特征,捕捉更全面脑结构信息。
- 在ADNI数据集上达到94.3%准确率,显著优于传统单平面方法。
- 揭示右侧皮层下结构不对称性变化,模型结果更具临床可解释性。
阿尔茨海默病(AD)是一种进行性神经退行性疾病,严重损害认知功能与生活质量。早期精准诊断对及时干预至关重要,但因脑部结构细微且复杂的变化而极具挑战。现有深度学习方法多仅基于单一平面的结构性磁共振成像(sMRI),难以准确捕捉病灶区域间的复杂非线性关系,限制了对萎缩特征的精确识别。为此,本文提出MPF-KANSC框架,结合多平面融合(MPF)与柯尔莫哥洛夫-阿诺德网络引导的空间-通道注意力机制(KANSC),实现对sMRI萎缩特征的高效学习与表达。模型并行提取三个解剖平面特征,增强结构信息完整性;KANSC利用更强的非线性函数逼近能力,精准定位疾病相关异常。在ADNI数据集上的实验表明,该方法在AD诊断任务中表现优异,准确率达94.3%。此外,研究发现右半球皮层下结构变化存在显著不对称性,凸显模型的可解释潜力。
原文摘要 · Abstract (English)
Alzheimer's disease (AD) is a progressive neurodegenerative disorder that severely impairs cognitive function and quality of life. Timely intervention in AD relies heavily on early and precise diagnosis, which remains challenging due to the complex and subtle structural changes in the brain. Most existing deep learning methods focus only on a single plane of structural magnetic resonance imaging (sMRI) and struggle to accurately capture the complex and nonlinear relationships among pathological regions of the brain, thus limiting their ability to precisely identify atrophic features. To overcome these limitations, we propose an innovative framework, MPF-KANSC, which integrates multi-plane fusion (MPF) for combining features from the coronal, sagittal, and axial planes, and a Kolmogorov-Arnold Network-guided spatial-channel attention mechanism (KANSC) to more effectively learn and represent sMRI atrophy features. Specifically, the proposed model enables parallel feature extraction from multiple anatomical planes, thus capturing more comprehensive structural information. The KANSC attention mechanism further leverages a more flexible and accurate nonlinear function approximation technique, facilitating precise identification and localization of disease-related abnormalities. Experiments on the ADNI dataset confirm that the proposed MPF-KANSC achieves superior performance in AD diagnosis. Moreover, our findings provide new evidence of right-lateralized asymmetry in subcortical structural changes during AD progression, highlighting the model's promising interpretability.
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