CoEN5025 NANOSYN: Unravelling synaptic pathology in Alzheimer's disease and Dementia with Lewy bodies using super-resolution microscopy

阿尔茨海默病(AD)和路易体痴呆(DLB)是导致痴呆的两个最常见的原因。为了找到有效的治疗方法，我们了解确切的原因是至关重要的。阿尔茨海默病患者大脑中Abeta和tau蛋白的积聚发生在早期。在DLB中，一种名为α-突触核蛋白的蛋白质在神经元内早期积聚。我们知道，突触，神经元之间最关键的交流结构，在这些疾病中很早就失去了。然而，由于缺乏足够的技术，这些蛋白质破坏突触的确切机制尚不清楚。在这里，我们将应用现有的最先进的工具来调查一组独特的人类大脑样本中突触上异常蛋白质的存在。我们还将研究有毒蛋白对突触组成的影响。这些信息将对开发针对两种最常见的痴呆症原因的更具体的治疗方法具有非常宝贵的价值。

Alzheimer's disease (AD) and Dementia with Lewy bodies (DLB) are the two most common causes of dementia. In order to find effective treatments, it is critical that we understand the exact causes. Accumulation of Abeta and tau proteins in the brain occurs early in people with AD. In DLB, a protein called alpha-synuclein accumulates early inside neurons. We know that synapses, the most critical structures for communication between neurons, are lost very early in these diseases. However, the precise mechanism by which these proteins damage synapses is poorly understood due to the lack of adequate techniques. Here, we will apply the most advanced tools available to investigate the presence of abnormal proteins at synapses in a unique set of human brain samples. We will also investigate the effects of toxic proteins on synapse composition. This information will be invaluable for the development of more specific treatments for the two most common causes of dementia.