Department of Radiology, University of California, San Francisco, San Francisco, California.
Department of Radiology, University of California, San Francisco, San Francisco, California.
Transl Res. 2023 Apr;254:13-23. doi: 10.1016/j.trsl.2022.08.008. Epub 2022 Aug 27.
With the increasing prevalence of Alzheimer's disease (AD) among aging populations and the limited therapeutic options available to slow or reverse its progression, the need has never been greater for improved diagnostic tools for identifying patients in the preclinical and prodomal phases of AD. Biophysics models of the connectome-based spread of amyloid-beta (Aβ) and microtubule-associated protein tau (τ) have enjoyed recent success as tools for predicting the time course of AD-related pathological changes. However, given the complex etiology of AD, which involves not only connectome-based spread of protein pathology but also the interactions of many molecular and cellular players over multiple spatiotemporal scales, more robust, complete biophysics models are needed to better understand AD pathophysiology and ultimately provide accurate patient-specific diagnoses and prognoses. Here we discuss several areas of active research in AD whose insights can be used to enhance the mathematical modeling of AD pathology as well as recent attempts at developing improved connectome-based biophysics models. These efforts toward a comprehensive yet parsimonious mathematical description of AD hold great promise for improving both the diagnosis of patients at risk for AD and our mechanistic understanding of how AD progresses.
随着老龄化人口中阿尔茨海默病(AD)的患病率不断上升,而可用的减缓或逆转其进展的治疗方法有限,因此,人们迫切需要改进诊断工具,以在 AD 的临床前和前驱期识别患者。基于连接组的淀粉样蛋白-β(Aβ)和微管相关蛋白 tau(τ)扩散的生物物理模型最近作为预测 AD 相关病理变化时间进程的工具取得了成功。然而,鉴于 AD 的复杂病因,它不仅涉及基于连接组的蛋白病理学扩散,还涉及许多分子和细胞成分在多个时空尺度上的相互作用,因此需要更强大、更完整的生物物理模型,以便更好地了解 AD 病理生理学,并最终提供准确的患者特异性诊断和预后。在这里,我们讨论了 AD 中几个活跃的研究领域,这些领域的研究可以用于增强 AD 病理学的数学建模,以及最近在开发改进的基于连接组的生物物理模型方面的尝试。这些朝着全面而简约的 AD 数学描述的努力为改善 AD 风险患者的诊断以及我们对 AD 进展方式的机制理解提供了巨大的希望。