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

Accumulation of beta-amyloid (Abeta) peptides in senile plaques is one of the pathological hallmarks in Alzheimer's disease (AD), which can trigger apoptosis. We have previously demonstrated that Abeta triggered calcium release from the ER. Depletion of ER Ca(2+) ions has been reported leading...

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Veröffentlicht in:	Apoptosis (London) 2006-05, Vol.11 (5), p.687-700
Hauptverfasser:	Yu, Man-Shan, Suen, Ka-Chun, Kwok, Nga-Sze, So, Kwok-Fai, Hugon, Jacques, Chang, Raymond Chuen-Chung
Format:	Artikel
Sprache:	eng
Schlagworte:	Accumulation Alzheimer's disease Amyloid beta-Peptides - chemistry Amyloid beta-Peptides - pharmacology Animals Apoptosis Apoptosis - drug effects Basic-Leucine Zipper Transcription Factors - metabolism Calcium ions Cell Culture Techniques Cells, Cultured Cerebral Cortex - cytology Cerebral Cortex - embryology CHOP protein Depletion DNA-Binding Proteins Neoplasm Proteins - metabolism Neurodegeneration Neurodegenerative diseases Neurons - cytology Neurons - drug effects Neurons - physiology Peptide Fragments - pharmacology Peptides Phosphorylation Protein Denaturation - physiology Protein folding Proteins Rats Rats, Sprague-Dawley Regulatory Factor X Transcription Factors RNA, Messenger - metabolism Senile plaques Time Factors Transcription Factors X-Box Binding Protein 1 β-Amyloid
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