Selective increase in cellular Aβ42 is related to apoptosis but not necrosis

Abstract

Amyloid beta protein ending at 42 (A beta 42) plays an important role in the pathology of Alzheimer's disease (AD). Here we show an increase in cellular A beta 42 in damaged neurons, with both ELISA and immunocytochemistry. The cellular A beta 42 increase was caused by 3-day treatments with H2O2, etoposide or melphalan, all of which induce genotoxic apoptosis, but not by treatment with sodium azide, which causes necrosis. Secreted A beta was similarly decreased with all these treatments. The cellular A beta 42 increase appeared even with minimal damage (ELISA) and A beta 42-positive cells were TUNEL negative (double staining), indicating that any early apoptosis mechanism may induce the cellular A beta 42 increase. Thus, neuronal apoptosis and cellular A beta 42 increase may be linked in a way that contributes importantly to AD pathology.

Keywords

ApoptosisImmunocytochemistryTUNEL assayBiologyBETA (programming language)Programmed cell deathNecrosisAmyloid betaCell biologyPathologyEndocrinologyMedicineBiochemistryGenetics

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Publication Info

Year: 2000
Type: article
Volume: 11
Issue: 1
Pages: 167-171
Citations: 69
Access: Closed

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APA Style

                            
                                
                                    Yasumasa Ohyagi, 
                                
                                    Takeshi Yamada, 
                                
                                    Kenichi Nishioka
                                
                                et al.
                            
                            (2000). 
                            Selective increase in cellular Aβ42 is related to apoptosis but not necrosis. 
                            Neuroreport
                            , 11
                            (1)
                            , 167-171.
                            https://doi.org/10.1097/00001756-200001170-00033
                        

Identifiers

DOI: 10.1097/00001756-200001170-00033