NDLI: Beta-amyloid peptides induces neuronal apoptosis via a mechanism independent of unfolded protein responses

Content Provider	Springer Nature Link
Author	Yu, Man Shan Suen, Ka Chun Kwok, Nga Sze So, Kwok Fai Hugon, Jacques Chang, Raymond
Copyright Year	2006
Abstract	Accumulation of beta-amyloid (Aβ) peptides in senile plaques is one of the pathological hallmarks in Alzheimer's disease (AD), which can trigger apoptosis. We have previously demonstrated that Aβ triggered calcium release from the ER. Depletion of ER Ca2+ ions has been reported leading to unfolded protein responses (UPR). While hypothesis has been made about UPR and neurodegeneration in AD, little is known about the effects of extracellular accumulation of Aβ on UPR. We have shown previously that activation of PKR in Aβ-triggered apoptosis. Since UPR can trigger PKR, our study aims to elucidate whether extracellular accumulation of Aβ peptides induce UPR in cultured neurons. Our results showed that Aβ could not trigger UPR signalings including phosphorylation of PERK, alternative cleavage of xbp-1 mRNA and induction of transcription of xbp-1 and Gadd153. Taken together, our results suggest that extracellular accumulation of Aβ peptides induce apoptosis via a mechanism independent of UPR.
Starting Page	687
Ending Page	700
Page Count	14
File Format	PDF
ISSN	13608185
Journal	Apoptosis
Volume Number	11
Issue Number	5
e-ISSN	1573675X
Language	English
Publisher	Kluwer Academic Publishers
Publisher Date	2006-03-09
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	apoptosis beta-amyloid calcium caspases unfolded protein responses Cancer Research Virology Oncology Biochemistry Cell Biology
Content Type	Text
Resource Type	Article
Subject	Pharmaceutical Science Biochemistry (medical) Cell Biology Clinical Biochemistry Cancer Research Pharmacology

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