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

Yasumasa Ohyagi; Takeshi Yamada; Kenichi Nishioka; Nigel J. Clarke; Andy J. Tomlinson; Stephen Naylor; Yusaku Nakabeppu; Jun Ichi Kira; Steven G. Younkin

doi:10.1097/00001756-200001170-00033

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

Yasumasa Ohyagi, Takeshi Yamada, Kenichi Nishioka, Nigel J. Clarke, Andy J. Tomlinson, Stephen Naylor, Yusaku Nakabeppu, Jun Ichi Kira, Steven G. Younkin

Neuroscience

Research output: Contribution to journal › Article › peer-review

65 Scopus citations

Abstract

Amyloid β protein ending at 42 (Aβ42) plays an important role in the pathology of Alzheimer's disease (AD). Here we show an increase in cellular Aβ42 in damaged neurons, with both ELISA and immunocytochemistry. The cellular Aβ42 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 Aβ was similarly decreased with all these treatments. The cellular Aβ42 increase appeared even with minimal damage (ELISA) and Aβ42-positive cells were TUNEL negative (double staining), indicating that any early apoptosis mechanism may induce the cellular Aβ42 increase. Thus, neuronal apoptosis and cellular Aβ42 increase may be linked in a way that contributes importantly to AD pathology.

Original language	English (US)
Pages (from-to)	167-171
Number of pages	5
Journal	NeuroReport
Volume	11
Issue number	1
DOIs	https://doi.org/10.1097/00001756-200001170-00033
State	Published - Jan 17 2000

Keywords

Amyloid β protein
Apoptosis
ELISA
Immunocytochemistry
Increase
Necrosis
Neuron

ASJC Scopus subject areas

Neuroscience(all)

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10.1097/00001756-200001170-00033

Cite this

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title = "Selective increase in cellular Aβ42 is related to apoptosis but not necrosis",

abstract = "Amyloid β protein ending at 42 (Aβ42) plays an important role in the pathology of Alzheimer's disease (AD). Here we show an increase in cellular Aβ42 in damaged neurons, with both ELISA and immunocytochemistry. The cellular Aβ42 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 Aβ was similarly decreased with all these treatments. The cellular Aβ42 increase appeared even with minimal damage (ELISA) and Aβ42-positive cells were TUNEL negative (double staining), indicating that any early apoptosis mechanism may induce the cellular Aβ42 increase. Thus, neuronal apoptosis and cellular Aβ42 increase may be linked in a way that contributes importantly to AD pathology.",

keywords = "Amyloid β protein, Apoptosis, ELISA, Immunocytochemistry, Increase, Necrosis, Neuron",

author = "Yasumasa Ohyagi and Takeshi Yamada and Kenichi Nishioka and Clarke, {Nigel J.} and Tomlinson, {Andy J.} and Stephen Naylor and Yusaku Nakabeppu and Kira, {Jun Ichi} and Younkin, {Steven G.}",

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T1 - Selective increase in cellular Aβ42 is related to apoptosis but not necrosis

AU - Ohyagi, Yasumasa

AU - Yamada, Takeshi

AU - Nishioka, Kenichi

AU - Clarke, Nigel J.

AU - Tomlinson, Andy J.

AU - Naylor, Stephen

AU - Nakabeppu, Yusaku

AU - Kira, Jun Ichi

AU - Younkin, Steven G.

PY - 2000/1/17

Y1 - 2000/1/17

N2 - Amyloid β protein ending at 42 (Aβ42) plays an important role in the pathology of Alzheimer's disease (AD). Here we show an increase in cellular Aβ42 in damaged neurons, with both ELISA and immunocytochemistry. The cellular Aβ42 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 Aβ was similarly decreased with all these treatments. The cellular Aβ42 increase appeared even with minimal damage (ELISA) and Aβ42-positive cells were TUNEL negative (double staining), indicating that any early apoptosis mechanism may induce the cellular Aβ42 increase. Thus, neuronal apoptosis and cellular Aβ42 increase may be linked in a way that contributes importantly to AD pathology.

AB - Amyloid β protein ending at 42 (Aβ42) plays an important role in the pathology of Alzheimer's disease (AD). Here we show an increase in cellular Aβ42 in damaged neurons, with both ELISA and immunocytochemistry. The cellular Aβ42 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 Aβ was similarly decreased with all these treatments. The cellular Aβ42 increase appeared even with minimal damage (ELISA) and Aβ42-positive cells were TUNEL negative (double staining), indicating that any early apoptosis mechanism may induce the cellular Aβ42 increase. Thus, neuronal apoptosis and cellular Aβ42 increase may be linked in a way that contributes importantly to AD pathology.

KW - Amyloid β protein

KW - Apoptosis

KW - ELISA

KW - Immunocytochemistry

KW - Increase

KW - Necrosis

KW - Neuron

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ER -

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

Abstract

Keywords

ASJC Scopus subject areas

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