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.
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