Xue Chonghua, Kowshik Sahana S, Lteif Diala, Puducheri Shreyas, Jasodanand Varuna H, Zhou Olivia T, Walia Anika S, Guney Osman B, Zhang J Diana, Pham Serena T, Kaliaev Artem, Andreu-Arasa V Carlota, Dwyer Brigid C, Farris Chad W, Hao Honglin, Kedar Sachin, Mian Asim Z, Murman Daniel L, O'Shea Sarah A, Paul Aaron B, Rohatgi Saurabh, Saint-Hilaire Marie-Helene, Sartor Emmett A, Setty Bindu N, Small Juan E, Swaminathan Arun, Taraschenko Olga, Yuan Jing, Zhou Yan, Zhu Shuhan, Karjadi Cody, Ang Ting Fang Alvin, Bargal Sarah A, Plummer Bryan A, Poston Kathleen L, Ahangaran Meysam, Au Rhoda, Kolachalama Vijaya B
Department of Medicine, Boston University Chobanian & Avedisian School of Medicine, Boston, MA, USA.
Department of Electrical & Computer Engineering, Boston University, MA, USA.
medRxiv. 2024 Mar 26:2024.02.08.24302531. doi: 10.1101/2024.02.08.24302531.
Differential diagnosis of dementia remains a challenge in neurology due to symptom overlap across etiologies, yet it is crucial for formulating early, personalized management strategies. Here, we present an AI model that harnesses a broad array of data, including demographics, individual and family medical history, medication use, neuropsychological assessments, functional evaluations, and multimodal neuroimaging, to identify the etiologies contributing to dementia in individuals. The study, drawing on 51,269 participants across 9 independent, geographically diverse datasets, facilitated the identification of 10 distinct dementia etiologies. It aligns diagnoses with similar management strategies, ensuring robust predictions even with incomplete data. Our model achieved a micro-averaged area under the receiver operating characteristic curve (AUROC) of 0.94 in classifying individuals with normal cognition, mild cognitive impairment and dementia. Also, the micro-averaged AUROC was 0.96 in differentiating the dementia etiologies. Our model demonstrated proficiency in addressing mixed dementia cases, with a mean AUROC of 0.78 for two co-occurring pathologies. In a randomly selected subset of 100 cases, the AUROC of neurologist assessments augmented by our AI model exceeded neurologist-only evaluations by 26.25%. Furthermore, our model predictions aligned with biomarker evidence and its associations with different proteinopathies were substantiated through postmortem findings. Our framework has the potential to be integrated as a screening tool for dementia in various clinical settings and drug trials, with promising implications for person-level management.
由于不同病因导致的症状重叠,痴呆症的鉴别诊断在神经学领域仍然是一项挑战,但对于制定早期、个性化的管理策略至关重要。在此,我们展示了一种人工智能模型,该模型利用广泛的数据,包括人口统计学、个人和家族病史、用药情况、神经心理学评估、功能评估以及多模态神经影像学,来识别导致个体痴呆症的病因。这项研究基于9个独立的、地理位置不同的数据集,涵盖51269名参与者,有助于识别出10种不同的痴呆症病因。它将诊断与相似的管理策略相结合,即使数据不完整也能确保可靠的预测。我们的模型在对认知正常、轻度认知障碍和痴呆症患者进行分类时,受试者工作特征曲线下的微平均面积(AUROC)达到了0.94。此外,在区分痴呆症病因时,微平均AUROC为0.96。我们的模型在处理混合性痴呆病例方面表现出色,对于两种同时存在的病理情况,平均AUROC为0.78。在随机选择的100个病例子集中,我们的人工智能模型增强后的神经科医生评估的AUROC比仅由神经科医生进行的评估高出26.25%。此外,我们的模型预测与生物标志物证据相符,并且通过尸检结果证实了其与不同蛋白质病变的关联。我们的框架有可能作为一种痴呆症筛查工具,整合到各种临床环境和药物试验中,对个人层面的管理具有广阔的应用前景。