Center for Neurologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA, USA.
Mol Neurodegener. 2009 Nov 23;4:48. doi: 10.1186/1750-1326-4-48.
Synapse loss is an early and invariant feature of Alzheimer's disease (AD) and there is a strong correlation between the extent of synapse loss and the severity of dementia. Accordingly, it has been proposed that synapse loss underlies the memory impairment evident in the early phase of AD and that since plasticity is important for neuronal viability, persistent disruption of plasticity may account for the frank cell loss typical of later phases of the disease. Extensive multi-disciplinary research has implicated the amyloid beta-protein (Abeta) in the aetiology of AD and here we review the evidence that non-fibrillar soluble forms of Abeta are mediators of synaptic compromise. We also discuss the possible mechanisms of Abeta synaptotoxicity and potential targets for therapeutic intervention.
突触丧失是阿尔茨海默病（AD）的早期和不变特征，突触丧失的程度与痴呆的严重程度之间存在很强的相关性。因此，有人提出，突触丧失是 AD 早期阶段明显记忆障碍的基础，由于可塑性对于神经元存活很重要，因此持续破坏可塑性可能是该疾病后期阶段典型的细胞大量丧失的原因。广泛的多学科研究表明β淀粉样蛋白（Abeta）与 AD 的病因有关，在这里我们回顾了非纤维状可溶性 Abeta 形式是突触损伤介质的证据。我们还讨论了 Abeta 突触毒性的可能机制和治疗干预的潜在靶点。
