Intraneuronal amyloid beta42 enhanced by heating but counteracted by formic acid.
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.
Ohyagi
Yasumasa
Y
Department of Neurology, Neurological Institute, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Fukuoka 812-8582, Japan. ohyagi@neuro.med.kyushu-u.ac.jp
Tsuruta
Yuko
Y
Motomura
Kyoko
K
Miyoshi
Katsue
K
Kikuchi
Hitoshi
H
Iwaki
Toru
T
Taniwaki
Takayuki
T
Kira
Jun-ichi
J
D000368:Aged; D000369:Aged, 80 and over; D000544:Alzheimer Disease / Q000378:metabolism; D016229:Amyloid beta-Peptides / Q000737:chemistry*; D000939:Epitopes; D005260:Female; D005561:Formates / Q000737:chemistry*; D006358:Hot Temperature; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D009474:Neurons / Q000737:chemistry*; D010446:Peptide Fragments / Q000737:chemistry*
D016229:Amyloid beta-Peptides; D000939:Epitopes; D005561:Formates; D010446:Peptide Fragments; C075222:amyloid beta-protein (1-42); C030544:formic acid