Capsoni Simona, Giannotta Sabina, Cattaneo Antonino
Neuroscience Program, International School for Advanced Studies (SISSA), Trieste, Italy.
Mol Cell Neurosci. 2002 Sep;21(1):15-28. doi: 10.1006/mcne.2002.1163.
Cerebral deposition of beta-amyloid (Abeta) is an invariant event of Alzheimer's disease (AD). We recently described that the brain of aged transgenic mice expressing anti-nerve growth factor (NGF) antibodies (AD11 mice) show a dramatic neurodegenerative phenotype, reminiscent of AD, which includes neuronal loss, cholinergic deficit, and tau hyperphosphorylation, associated with neurofibrillary pathology. We now report that brains of aged transgenic mice contain large amounts of beta-amyloid plaques and describe their morphology by a variety of approaches. In conclusion, the chronic deprivation of NGF leads to the formation and deposition of Abeta in AD11 mice, suggesting a direct link between NGF signaling and abnormal processing of amyloid precursor protein.
β-淀粉样蛋白（Aβ）在大脑中的沉积是阿尔茨海默病（AD）的一个不变事件。我们最近描述了表达抗神经生长因子（NGF）抗体的老年转基因小鼠（AD11小鼠）的大脑表现出显著的神经退行性表型，类似于AD，包括神经元丢失、胆碱能缺陷和tau蛋白过度磷酸化，并伴有神经原纤维病理改变。我们现在报告老年转基因小鼠的大脑中含有大量β-淀粉样斑块，并通过多种方法描述了它们的形态。总之，NGF的长期缺乏导致AD11小鼠中Aβ的形成和沉积，提示NGF信号传导与淀粉样前体蛋白的异常加工之间存在直接联系。
