Intraneuronal amyloid β42 enhanced by heating but counteracted by formic acid
Intraneuronal amyloid β42 enhanced by heating but counteracted by formic acid
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DOI：
10.1016/j.jneumeth.2006.06.010
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发表时间：
2007-01
影响因子：
3
通讯作者：
Y. Ohyagi;Y. Tsuruta;K. Motomura;Katsue Miyoshi;H. Kikuchi;T. Iwaki;T. Taniwaki;J. Kira
中科院分区：
文献类型：
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作者：
Y. Ohyagi;Y. Tsuruta;K. Motomura;Katsue Miyoshi;H. Kikuchi;T. Iwaki;T. Taniwaki;J. Kira
A β 42（Amyloid β-protein ending at 42，Aβ42）是阿尔茨海默病（Alzheimer's disease，AD）患者脑内沉积的主要多肽。在免疫细胞化学研究中，甲酸处理可显著增强Aβ免疫反应性。最近，有报道称Aβ42在AD神经元中蓄积。由于已知加热可增强细胞内蛋白免疫反应性，因此我们使用高压灭菌方案来增强神经元内Aβ42免疫反应性。使用该方案，抗A β42 N-末端和C-末端抗体，但不抗A β40 C-末端抗体，标记AD神经元。此外，甲酸处理抵消了高压灭菌的这种影响。因此，仅使用甲酸的常规方法可能低估了神经元内Aβ42的蓄积。
Amyloid β-protein ending at 42 (Aβ42) is the major peptide deposited in Alzheimer's disease (AD) brain. In immunocytochemical studies, formic acid treatment is used to dramatically enhance Aβ immunoreactivity. Recently, Aβ42 has been reported to accumulate in AD neurons. Since heating is known to enhance intracellular protein immunoreactivity, we used an autoclaving protocol to enhance intraneuronal Aβ42 immunoreactivity. Using this protocol, both anti-Aβ42 N-terminal and C-terminal antibodies, but not anti-Aβ40 C-terminal antibody, labeled AD neurons. Moreover, formic acid treatment counteracted such effects of autoclaving. Thus, intraneuronal Aβ42 accumulation may have been underestimated by conventional methods using formic acid only.