Intraneuronal amyloid β42 enhanced by heating but counteracted by formic acid

Amyloid beta-protein ending at 42 (A beta 42) is the major peptide deposited in Alzheimer's disease (AD) brain. In immunocytochemical studies, formic acid treatment is used to dramatically enhance A beta immunoreactivity. Recently, A beta 42 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 A beta 42 immunoreactivity. Using this protocol, both anti-A beta 42 N-terminal and C-terminal antibodies, but not anti-A beta 40 C-terminal antibody, labeled AD neurons. Moreover, formic acid treatment counteracted such effects of autoclaving. Thus, intraneuronal A beta 42 accumulation may have been underestimated by conventional methods using formic acid only. (c) 2006 Elsevier B.V. All rights reserved.