Investigating aberrant neuronal calcium regulation by calpain in Alzheimer s Disease

患有阿尔茨海默病（AD）的人有严重的记忆丧失和痴呆。这些症状是由大脑中用于记忆、识别和大多数赋予我们个性的大脑功能的神经细胞的持续而无情的死亡引起的。我的研究目的是调查为什么神经细胞在阿尔茨海默病中死亡，因为如果我们能防止这种细胞死亡，那么我们就能有效地治疗这种毁灭性的疾病。我将重点关注增加神经细胞内钙含量的事件。正常情况下，进入和离开神经细胞的钙量是平衡的，但在阿尔茨海默病中，这一过程被破坏，神经细胞内过量的钙导致它们死亡。我的项目将调查这种钙失衡的原因。我还将使用动物模型来测试应该恢复钙平衡的药物的有效性，以确定它们是否可以防止神经细胞死亡，这是AD的特征。这项工作可能会导致一种治疗阿尔茨海默病的新策略，可以由制药行业开发，并可能导致新一代治疗这种毁灭性疾病的方法。

People who suffer from Alzheimer’s disease (AD) have severe memory loss and dementia. These symptoms are caused by the progressive and relentless death of nerve cells in the brain that we use for memory, recognition and most brain functions that give us our personality. My research is aimed at investigating why nerve cells die in AD because if we can prevent this cell death then we will have effective treatments for this devastating condition. I will focus on events that increase the amount of calcium inside nerve cells. Normally there is a balance between the amount of calcium entering and leaving nerve cells, but in AD this process is disrupted and excess calcium inside nerve cells causes them to die. My project will investigate the reasons for this calcium imbalance. I will also use animal models to test the effectiveness of drugs that should restore the calcium balance to determine whether they can prevent the nerve cell death that is characteristic of AD. This work may lead to a new strategy for treating AD which can be developed by the pharmaceutical industry and could result in a new generation of treatments for this devastating illness.