Synapse dysfunction is an integral feature of Alzheimer’s disease (AD) pathophysiology. In fact, prodromal manifestation of structural and functional deficits in synapses much prior to appearance of overt pathological hallmarks of the disease indicates that AD might be considered as a degenerative disorder of the synapses. Several research instruments and techniques have allowed us to study synaptic function and plasticity and their alterations in pathological conditions, such as AD. One such tool is the biochemically isolated preparations of detached and resealed synaptic terminals, the “synaptosomes”. Because of the preservation of many of the physiological processes such as metabolic and enzymatic activities, synaptosomes have proved to be an indispensable ex vivo model system to study synapse physiology both when isolated from fresh or cryopreserved tissues, and from animal or human post-mortem tissues. This model system has been tremendously successful in the case of post-mortem tissues because of their accessibility relative to acute brain slices or cultures. The current review details the use of synaptosomes in AD research and its potential as a valuable tool in furthering our understanding of the pathogenesis and in devising and testing of therapeutic strategies for the disease.

突触功能障碍是阿尔茨海默病 (AD) 病理生理学的一个组成部分。事实上，在疾病的明显病理特征出现之前，突触中结构和功能缺陷的前驱表现表明 AD 可能被认为是突触的一种退行性疾病。一些研究仪器和技术使我们能够研究突触功能和可塑性及其在病理条件下的改变，例如 AD。一种这样的工具是分离和重新密封的突触末端的生化分离制剂，即“突触体”。由于保留了许多生理过程，例如代谢和酶活性，突触体已被证明是必不可少的离体用于研究从新鲜或冷冻保存的组织以及动物或人类死后组织中分离时的突触生理学的模型系统。该模型系统在死后组织的情况下取得了巨大的成功，因为它们相对于急性脑切片或培养物的可访问性。目前的综述详细介绍了突触体在 AD 研究中的应用及其作为一种有价值的工具的潜力，可进一步加深我们对发病机制的理解，并设计和测试该疾病的治疗策略。