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Intraneuronal Amyloid β42 Enhanced by Heating but Counteracted by Formic Acid by Yasumasa Ohyagi; Yuko Tsuruta; Kyoko Motomura; Katsue Miyoshi; Hitoshi Kikuchi; Toru Iwaki; Takayuki Taniwaki; Jun-ichi Kira is a Neuroscience article available to read on EtoBox.

What is Intraneuronal Amyloid β42 Enhanced by Heating but Counteracted by Formic Acid about?

Amyloid beta-protein ending at 42 (Abeta42) is the major peptide deposited in Alzheimer's disease (AD) brain. In immunocytochemical studies, formic acid treatment is used to dramatically enhance Abeta immunoreactivity. Recently, Abeta42 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 Abeta42 immunoreactivity. Using this protocol, both anti-Abeta42 N-terminal and C-terminal antibodies, but not anti-Abeta40 C-terminal antibody, labeled AD neurons. Moreover, formic acid treatment counteracted such effects of autoclaving. Thus, intraneuronal Abeta42 accumulation may have been underestimated by conventional methods using formic acid only.

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Author

Yasumasa Ohyagi; Yuko Tsuruta; Kyoko Motomura; Katsue Miyoshi; Hitoshi Kikuchi; Toru Iwaki; Takayuki Taniwaki; Jun-ichi Kira

Publisher

Elsevier Science; Elsevier ; Elsevier BV (ISSN 0165-0270)

Published

2007

Language

EN

Field

Neuroscience (Life Sciences)