Presenilin-1 mutations downregulate the signalling pathway of the unfolded-protein response. - AlzForum Alzheimer Research Paper of the Week


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Home: Papers of the Week

Annotation

	Katayama T, Imaizumi K, Sato N, Miyoshi K, Kudo T, Hitomi J, Morihara T, Yoneda T, Gomi F, Mori Y, Nakano Y, Takeda J, Tsuda T, Itoyama Y, Murayama O, Takashima A, St George-Hyslop P, Takeda M, Tohyama M. Presenilin-1 mutations downregulate the signalling pathway of the unfolded-protein response. Nat Cell Biol. 1999 Dec;1(8):479-85. PubMed Abstract

	Comments on Paper and Primary News

	Comment by: Hiroshi Mori, ARF Advisor
	Permalink
	This is a nice cell biological study on AD. Perturbation at ER documented here is deeply related with all types of AD. Further investigation is welcome. View all comments by Hiroshi Mori

	Comment by: Nikolaos K. Robakis
	Permalink
	This is an important paper as it reports a new PS1 function and suggests a mechanism for cellular damage of the PS1 FAD mutations. View all comments by Nikolaos K. Robakis

	Comments on Related Papers

	Related Paper: Disturbed activation of endoplasmic reticulum stress transducers by familial Alzheimer's disease-linked presenilin-1 mutations. Comment by: Benjamin Wolozin, ARF Advisor (Disclosure)
	Permalink
	I recommend this paper The ER appears to be a critical site for stress in neurodegenerative diseases. Several of the proteins that are implicated in neurodegenerative disease are present in the ER, and affect ER stress responses. Our understanding of the mechanism by which proteins, such as PS1, affect ER stress signaling could provide important insights into understanding the mechanism of disease. View all comments by Benjamin Wolozin

	Related Paper: Disturbed activation of endoplasmic reticulum stress transducers by familial Alzheimer's disease-linked presenilin-1 mutations. Comment by: Eddie Koo, ARF Advisor
	Permalink
	I recommend this paper Still more confusion about the upr and presenilins. Initial defects in upr reported for presenilins not confirmed by Thinakaran lab. View all comments by Eddie Koo

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