Senile Degeneration in the Brain of Octogon Degus

阿尔茨海默病(AD)是最常见的神经退行性疾病，其特点是进行性 记忆丧失和大脑皮层大量细胞死亡。对阿尔茨海默病病因的主要观点是 淀粉样蛋白积聚是导致神经退行性变的重要事件。这一假设得到了支持 人淀粉样前体蛋白(APP)家族突变转基因小鼠的研究 和早衰者。这些动物复制疾病的关键方面，包括淀粉样斑块，缺陷 认知任务和突触可塑性机制中的异常负责学习和 记忆。然而，这些小鼠很少出现神经生物膜缠结，突触和神经元也很少。 失落，公元后的标志。此外，这些家族性阿尔茨海默病模型的研究意义可能较小 散发性(非家族性)AD，约占AD病例的95%。我们将研究其可行性。 使用啮齿动物Ocdon des作为模型来研究散发性阿尔茨海默病。奥特登·德古斯，是一种昼夜活动， 视觉和高度社会化的啮齿动物，自然发展为类似AD的病理，包括淀粉样斑块和 随着年龄的增长，神经纤毛缠绕堆积。Ocdon des也表现出明显的与年龄相关的下降 辨别新奇和熟悉物体的能力，这是一项有效的视觉记忆任务。我们假设 类AD病理的发展改变了突触的可塑性和视觉记忆。为了测试 在这一假说中，我们建议确定在个体中o.deus是否存在认知障碍的程度 与突触可塑性缺陷和抗体沉积有关。这些调查可以建立一个 散发性阿尔茨海默病的动物模型将补充现有的家族性疾病模型。

Alzheimer disease (AD) is the most common neurodegenerative disease, characterized by progressive memory loss and massive cell death in the cerebral cortex. A predominant view of the cause of AD is that the amyloid accumulation is the essential event leading to neurodegeneration. This hypothesis is supported by research on transgenic mice expressing familial mutations of the human amyloid precursor protein (APP) and presenilins. These animals reproduce key aspects of the disease, including amyloid plaques, deficits in cognitive tasks and abnormalities in the mechanisms of synaptic plasticity responsible for learning and memory. However, these mice rarely develop neurobibrillary tangles and exhibit little synaptic and neuronal loss, hallmarks of AD. In addition, these models of familial forms of AD might be less significant to study sporadic (non-familial) forms of AD, which represent about 95% of AD cases. We will examine the feasibility of using the rodent Octodon degus as a model to study sporadic forms of AD. Octodon degus, is a diurnal, visual and highly social rodent that naturally develop AD-like pathologies including amyloid plaques and neurobrillary tangles accumulation with age. Octodon degus also exhibit a marked age-related decline in the ability to discriminate novel from familiar objects, a working visual memory task. We hypothesize that the development of AD-like pathologies in O.degus alters synaptic plasticity and impairs visual memory. To test this hypothesis, we propose to determine in individual O. degus whether the degree of cognitive impairments correlates with deficits in synaptic plasticity and the Ab deposits. These investigations could establish an animal model for sporadic AD that will complement existing models of familial forms of the disease.