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首页> 外文期刊>Human Genetics >Association of butyrylcholinesterase K variant with cholinesterase-positive neuritic plaques in the temporal cortex in late-onset Alzheimer's disease.
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Association of butyrylcholinesterase K variant with cholinesterase-positive neuritic plaques in the temporal cortex in late-onset Alzheimer's disease.

机译:迟发性阿尔茨海默氏病颞叶皮质中丁酰胆碱酯酶K变体与胆碱酯酶阳性神经炎斑块的相关性。

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摘要

In confirmed late-onset (>65 years) Alzheimer's disease, we found a greater load, both of overall neuritic plaques and of cholinesterase-positive neuritic plaques, in the temporal cortex of carriers of the butyrylcholinesterase K variant (BCHE-K) aged <80 years than of all other patients. The differences were most striking in the case of cholinesterase-positive neuritic plaques. Among BCHE-K carriers, densities of such plaques were over six times higher in patients <80 years at death than in those >80 years (P=0.01). Furthermore, in subjects <80 years, BCHE-K carriers had nearly six-fold greater densities of these plaques than non-carriers (P=0.009). We consider three potential explanations for these findings: that the K variant binds more readily to plaque constituents, that it promotes fibril formation or that it induces aberrant neurite growth.
机译:在已确诊的晚期(> 65岁)阿尔茨海默氏病中,我们发现年龄<的丁酰胆碱酯酶K变异体(BCHE-K)携带者的颞皮质中,总的神经斑块和胆碱酯酶阳性的神经斑块的负荷更大比所有其他患者高80岁。胆碱酯酶阳性神经炎性斑块的差异最明显。在BCHE-K携带者中,死于80岁以下的患者的斑块密度是80岁以上患者的六倍(P = 0.01)。此外,在<80岁的受试者中,BCHE-K携带者的斑块密度比非携带者高近六倍(P = 0.009)。我们考虑这些发现的三种可能的解释:K变体更容易结合噬斑成分,它促进原纤维形成或诱导异常的神经突生长。

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