Induction of the unfolded protein response and cell death pathway in Alzheimer's disease, but not in aged Tg2576 mice.

摘要: The endoplasmic reticulum (ER) stress results from disrupted protein folding triggered by mutation or oxidation, reduced proteasome activity, and altered Ca2+ homeostasis. ER is accompanied activation of the unfolded response (UPR) cell death pathway. We examined if UPR pathway would be activated in Alzheimer's disease (AD). RT-PCR experiments revealed increased splicing X-box binding protein-1 (XBP-1), an transcription factor, AD compared with age-matched control. Among target genes XBP-1, expression disulfide isomerase (PDI), but not glucose-regulated 78 (GRP78), was AD, suggesting disturbed AD. C/EBP homologous (CHOP), caspase-3, caspase-4, caspase-12, downstream mediators pathway, were Neither nor induced aged Tg2576 mice, a transgenic mouse model that reveals both plaque pathology some cognitive deficits. present study suggests induction pro-apoptotic proteins contribute to neuropathological process irrespective amyloid β senile plaque.