arXiv:2606. 15784v1 Announce Type: new Abstract: Alzheimer's disease (AD) progression is often described through the amyloid-tau-neurodegeneration, or AT(N), cascade.
By Nguyen Linh Dan Le
arXiv:2606. 17867v1 Announce Type: cross Abstract: Despite increasing adoption of multimodal approaches in Alzheimer's Disease (AD) research -- aimed at integrating molecular, structural, clinical, and genetic biomarkers to enhance disease characterization -- the relationships among these modalities remain poorly understood.
By Antonio Scardace, Daniele Rav\`i
arXiv:2606. 04066v1 Announce Type: cross Abstract: Understanding how structural connections are associated with tau propagation in Alzheimer's disease (AD) remains a central open question, yet existing computational models either rely heavily on biophysical assumptions or lack neurobiologically interpretable pathway maps.
By Jing Zhang, Norman Scheel, Minheng Chen, Tong Chen, Yanjun Lyu, David C. Zhu, Rong Zhang, Dajiang Zhu
arXiv:2606. 09671v1 Announce Type: cross Abstract: Alzheimer's disease (AD) progression is highly heterogeneous and is typically observed through sparse and irregular longitudinal data, posing challenges for prediction and personalised monitoring.
By Yinyu Huang, Yilin Zhang, Sofia Michopoulou, Christopher Kipps, Rahman Attar
arXiv:2606. 18535v1 Announce Type: cross Abstract: Multi-cause observational studies contain information about unmeasured confounding through the dependence structure among causes.
By Yordan P. Raykov, Hengrui Luo, Justin D. Strait, Wasiur R. KhudaBukhsh
Longitudinal modelling of Alzheimer's disease progression is clinically useful only if it can describe not just the most likely next diagnosis, but how a patient may evolve over time and how reliable that forecast is. Most deep learning approaches reduce this problem to single-step classification, treating cognitively normal, mild cognitive impairment, and dementia as flat categories while providing limited insight into how uncertainty accumulates across future visits.