The current meta-analysis of the cohort review was designed to elucidate the progress made in neuroproteomics of the synaptosome. The association of the comprehensive synaptic proteome and its link to physiological or pathological setting is rapidly mounting. Chemical synapses in the brain are focal hot spots for interneuronal signalling, signal transduction, and its plasticity. Structurally, synapses comprise axon termini or the presynapse (vesicles filled with neurotransmitters that function as molecular signals), synaptic clefts (extracellular matrix and adhesion molecules), and Postsynaptic Density or PSD (with receptors for neurotransmitters that rely upon the chemical signalling). The pre- and post-synaptic clefts are responsible for mediating and regulating neurotransmitter release, their receptor binding, and perception rely on chemical signals. Moreover, short- and long-term structural and functional alterations that are necessary for the optimal higherorder brain functions are also mainly dependent on the protein dynamics at the synapses. Not surprisingly, disruptions in synaptic physiology are considered as the major pathogenic mechanisms underlying the progression of several neurodegenerative disorders, including Alzheimer's disease. This review briefly discusses the subcellular fractionation protocols and the related biochemical approaches for the isolation of synaptic compartments. Besides, it discusses the progress made in understanding the pathological alterations in the synaptic proteome in neurodegenerative disorders, particularly focussing on Alzheimer's disease dementia.

目前对队列回顾的荟萃分析旨在阐明突触体神经蛋白质组学的进展。综合突触蛋白质组的关联及其与生理或病理环境的联系正在迅速增加。大脑中的化学突触是神经元间信号传导、信号转导及其可塑性的焦点。在结构上，突触包括轴突末端或突触前（充满作为分子信号的神经递质的囊泡）、突触间隙（细胞外基质和粘附分子）和突触后密度或 PSD（具有依赖于化学信号传导的神经递质的受体）。突触前和突触后间隙负责介导和调节神经递质释放、它们的受体结合、感知依赖于化学信号。此外，最佳高阶大脑功能所必需的短期和长期结构和功能改变也主要取决于突触处的蛋白质动力学。毫不奇怪，突触生理学的破坏被认为是几种神经退行性疾病（包括阿尔茨海默病）进展的主要致病机制。本综述简要讨论了突触隔室分离的亚细胞分离方案和相关的生化方法。此外，它还讨论了在了解神经退行性疾病中突触蛋白质组的病理变化方面取得的进展，特别是关注阿尔茨海默病痴呆。最佳高阶大脑功能所必需的短期和长期结构和功能改变也主要取决于突触处的蛋白质动力学。毫不奇怪，突触生理学的破坏被认为是几种神经退行性疾病（包括阿尔茨海默病）进展的主要致病机制。本综述简要讨论了突触隔室分离的亚细胞分离方案和相关的生化方法。此外，它还讨论了在了解神经退行性疾病中突触蛋白质组的病理变化方面取得的进展，特别是关注阿尔茨海默病痴呆。最佳高阶大脑功能所必需的短期和长期结构和功能改变也主要取决于突触处的蛋白质动力学。毫不奇怪，突触生理学的破坏被认为是几种神经退行性疾病（包括阿尔茨海默病）进展的主要致病机制。本综述简要讨论了突触隔室分离的亚细胞分离方案和相关的生化方法。此外，它还讨论了在了解神经退行性疾病中突触蛋白质组的病理变化方面取得的进展，特别是关注阿尔茨海默病痴呆。突触生理学的中断被认为是导致包括阿尔茨海默病在内的几种神经退行性疾病进展的主要致病机制。本综述简要讨论了突触隔室分离的亚细胞分离方案和相关的生化方法。此外，它还讨论了在了解神经退行性疾病中突触蛋白质组的病理变化方面取得的进展，特别是关注阿尔茨海默病痴呆。突触生理学的中断被认为是导致包括阿尔茨海默病在内的几种神经退行性疾病进展的主要致病机制。本综述简要讨论了突触隔室分离的亚细胞分离方案和相关的生化方法。此外，它还讨论了在了解神经退行性疾病中突触蛋白质组的病理变化方面取得的进展，特别是关注阿尔茨海默病痴呆。