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

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

69 Citations (Scopus)

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
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
Publication status	Published - Jan 17 2000

All Science Journal Classification (ASJC) codes

Neuroscience(all)

Access to Document

10.1097/00001756-200001170-00033

Cite this

@article{8507888e94f44f279ee7de5119d63515,

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.",

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.}",

year = "2000",

month = jan,

day = "17",

doi = "10.1097/00001756-200001170-00033",

language = "English",

volume = "11",

pages = "167--171",

journal = "NeuroReport",

issn = "0959-4965",

publisher = "Lippincott Williams and Wilkins",

number = "1",

}

TY - JOUR

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.

UR - http://www.scopus.com/inward/record.url?scp=0038578900&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0038578900&partnerID=8YFLogxK

U2 - 10.1097/00001756-200001170-00033

DO - 10.1097/00001756-200001170-00033

M3 - Article

C2 - 10683851

AN - SCOPUS:0038578900

SN - 0959-4965

VL - 11

SP - 167

EP - 171

JO - NeuroReport

JF - NeuroReport

IS - 1

ER -

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

Abstract

All Science Journal Classification (ASJC) codes

Access to Document

Other files and links

Fingerprint

Cite this