The development of biomarkers for Alzheimer disease (AD) has led to the origin of suspected non-AD pathophysiology (SNAP) — a heterogeneous biomarker-based concept that describes individuals with normal amyloid and abnormal tau and/or neurodegeneration biomarker status. In this Review, we describe the origins of the SNAP construct, along with its prevalence, diagnostic and prognostic implications, and underlying neuropathology. As we discuss, SNAP can be operationalized using different biomarker modalities, which could affect prevalence estimates and reported characteristics of SNAP in ways that are not yet fully understood. Moreover, the underlying aetiologies that lead to a SNAP biomarker profile, and whether SNAP is the same in people with and without cognitive impairment, remains unclear. Improved insight into the clinical characteristics and pathophysiology of SNAP is of major importance for research and clinical practice, as well as for trial design to optimize care and treatment of individuals with SNAP.

阿尔茨海默病 (AD) 生物标志物的开发导致了疑似非 AD 病理生理学 (SNAP) 的起源，这是一种基于异质生物标志物的概念，描述了具有正常淀粉样蛋白和异常 tau 和/或神经退行性生物标志物状态的个体。在这篇综述中，我们描述了 SNAP 结构的起源、其流行率、诊断和预后意义以及潜在的神经病理学。正如我们所讨论的，SNAP 可以使用不同的生物标志物模式进行操作，这可能会以尚未完全理解的方式影响 SNAP 的患病率估计和报告的特征。此外，导致 SNAP 生物标志物谱的根本病因学，以及 SNAP 在有和没有认知障碍的人中是否相同，仍不清楚。更好地了解 SNAP 的临床特征和病理生理学对于研究和临床实践以及优化 SNAP 患者护理和治疗的试验设计至关重要。