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首页> 外文期刊>Neuron >Abeta plaques lead to aberrant regulation of calcium homeostasis in vivo resulting in structural and functional disruption of neuronal networks.
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Abeta plaques lead to aberrant regulation of calcium homeostasis in vivo resulting in structural and functional disruption of neuronal networks.

机译：Abeta斑块导致体内钙稳态的异常调节，导致神经网络的结构和功能破坏。

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摘要

Alzheimer's disease is characterized by the deposition of senile plaques and progressive dementia. The molecular mechanisms that couple plaque deposition to neural system failure, however, are unknown. Using transgenic mouse models of AD together with multiphoton imaging, we measured neuronal calcium in individual neurites and spines in vivo using the genetically encoded calcium indicator Yellow Cameleon 3.6. Quantitative imaging revealed elevated [Ca(2+)]i (calcium overload) in approximately 20% of neurites in APP mice with cortical plaques, compared to less than 5% in wild-type mice, PS1 mutant mice, or young APP mice (animals without cortical plaques). Calcium overload depended on the existence and proximity to plaques. The downstream consequences included the loss of spinodendritic calcium compartmentalization (critical for synaptic integration) and a distortion of neuritic morphologies mediated, in part, by the phosphatase calcineurin. Together, these data demonstrate that senile plaques impair neuritic calcium homeostasis in vivo and result in the structural and functional disruption of neuronal networks.
机译：阿尔茨海默氏病的特征在于老年斑的沉积和进行性痴呆。然而，将斑块沉积与神经系统衰竭耦合的分子机制尚不清楚。使用AD的转基因小鼠模型和多光子成像，我们使用遗传编码的钙指示剂Yellow Cameleon 3.6在体内测量了单个神经突和棘中的神经元钙。定量成像显示，在具有皮质斑块的APP小鼠中，约20％的神经突中[Ca（2 +）] i（钙超载）升高，而在野生型小鼠，PS1突变型小鼠或年轻的APP小鼠中，不到[5％]没有皮质斑块的动物）。钙超载取决于斑块的存在和接近程度。下游的后果包括丧失了刺突树突状钙的分区（对突触整合至关重要）和部分由磷酸酶钙调神经磷酸酶介导的神经形态变形。总之，这些数据表明，老年斑在体内损害了神经钙稳态，并导致神经网络的结构和功能破坏。

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