Alzheimer's disease (AD) is defined by a deficiency in specific behavioural and/or cognitive domains, pointing to selective vulnerabilities of specific neurons from different brain regions. These vulnerabilities can be compared across neuron subgroups to identify the most vulnerable neuronal types, regions, and time points for further investigation. Thus, the relevant organizational frameworks for brain subgroups will hold great values for a clear understanding of the progression in AD. Presently, the neuronal vulnerability has yet urgently required to be elucidated as not yet been clearly defined. It is suggested that cell-autonomous and non-cell-autonomous mechanisms can affect the neuronal vulnerability to stressors, and in turn modulates AD progression. This review examines cell-autonomous and non-cell-autonomous mechanisms that contribute to the neuronal vulnerability. Collectively, the cell-autonomous mechanisms seem to be the primary drivers responsible for initiating specific stressor-related neuronal vulnerability with pathological changes in certain brain areas, which then utilize non-cell-autonomous mechanisms and result in subsequent progression of AD. In summary, this article has provided a new perspective on the preventative and therapeutic options for AD.

阿尔茨海默氏病（AD）的定义是特定行为和/或认知域的缺陷，指出来自不同大脑区域的特定神经元的选择性脆弱性。可以在各个神经元亚组之间比较这些漏洞，以确定最脆弱的神经元类型，区域和时间点，以进行进一步调查。因此，有关脑亚组的相关组织框架将具有巨大的价值，可清楚地了解AD的进展。目前，由于尚未明确定义，急需阐明神经元脆弱性。提出细胞自主和非细胞自主机制可以影响神经元对应激源的脆弱性，进而调节AD的进程。这项审查审查了导致神经元脆弱性的细胞自主和非细胞自主机制。总的来说，细胞自主机制似乎是引发特定脑应激相关神经元易损性的主要驱动力，其中某些大脑区域发生病理变化，然后利用非细胞自主机制导致AD的后续发展。总之，本文为AD的预防和治疗选择提供了新的视角。