Author(s):
Pereira, Cláudia 
; Ferreiro, Elisabete ; Cardoso, Sandra ; Oliveira, Catarina de
Date: 2004
Persistent ID: http://hdl.handle.net/10316/8503
Origin: Estudo Geral - Universidade de Coimbra
Document details
Cell degeneration induced by amyloid-ß peptides
Description
Abstract Extracellular accumulation of amyloid-ß (Aß) peptide and death of neurons in brain regions involved in learning and memory, particularly the cortex and the hippocampus, are central features of Alzheimer’s disease (AD). Neuronal Ca2+ overload and apoptosis are known to occur in AD. Aß might play a role in disrupting Ca2+ homeostasis, and this AD-associated amyloidogenic peptide has been reported to induce apoptotic death in cultured cells. However, the specific intracellular signaling pathways by which Aß triggers cell death are not yet well defined. This article provides evidence for the involvement of mitochondrial dysfunction in Aß-induced toxicity and for the role of mitochondria in apoptotsis triggered by Aß. In addition, the endoplasmic reticulum (ER) seems to play a role in Aß-induced apoptotic neuronal death, the ER stress being mediated by the perturbation of ER Ca2+ homeostasis. It is likely that a better understanding of how Aß induces neuronal apoptosis will lead to the identification of potential molecular targets for the development of therapies for AD. http://dx.doi.org/10.1385/JMN:23:1-2:097
Abstract Extracellular accumulation of amyloid-ß (Aß) peptide and death of neurons in brain regions involved in learning and memory, particularly the cortex and the hippocampus, are central features of Alzheimer’s disease (AD). Neuronal Ca2+ overload and apoptosis are known to occur in AD. Aß might play a role in disrupting Ca2+ homeostasis, and this AD-associated amyloidogenic peptide has been reported to induce apoptotic death in cultured cells. However, the specific intracellular signaling pathways by which Aß triggers cell death are not yet well defined. This article provides evidence for the involvement of mitochondrial dysfunction in Aß-induced toxicity and for the role of mitochondria in apoptotsis triggered by Aß. In addition, the endoplasmic reticulum (ER) seems to play a role in Aß-induced apoptotic neuronal death, the ER stress being mediated by the perturbation of ER Ca2+ homeostasis. It is likely that a better understanding of how Aß induces neuronal apoptosis will lead to the identification of potential molecular targets for the development of therapies for AD. http://dx.doi.org/10.1385/JMN:23:1-2:097
Document Type
Article
Language English
Language English
| Financiadores do RCAAP | |||||||
|
|
|
|
|
|
||