Neurovascular dysfunction arising from endothelial cell damage is an early pathogenic event that contributes to the neurodegenerative process occurring in Alzheimer's disease (AD). Since the mechanisms underlying endothelial dysfunction are not fully elucidated, this study was aimed to explore the hypothesis that brain endothelial cell death is induced upon the sustained activation of the endoplasmic reticulum ...
http://www.sciencedirect.com/science/article/B6T0F-4SSY90W-1/1/0b10903f573d4beaec42f0dc791857e3
In this study, we analyzed whether ER Ca2+ release, induced by amyloid-[beta] (A[beta]) and prion (PrP) peptides activates the mitochondrial-mediated apoptotic pathway. In cortical neurons, addition of the synthetic A[beta]1-40 or PrP106-126 peptides depletes ER Ca2+ content, leading to cytosolic Ca2+ overload. The Ca2+ released through ryanodine (RyR) and inositol 1,4,5-trisphosphate (IP3R) receptors was shown...
Intracellular neurofibrillary tangles, one of the characteristic hallmarks of Alzheimer's disease (AD), are mainly composed of hyperphosphorylated tau. The abnormal tau phosphorylation seems to be related to altered activity of kinases such as glycogen synthase kinase-3beta (GSK-3beta). Tau pathology is thought to be a later event during the progression of the disease, and it seems to occur as a consequence of ...
Prion (PrP) and amyloid-[beta] (A[beta]) peptides are involved in the neuronal loss that occurs in Prion disorders (PrD) and Alzheimer's disease (AD), respectively, partially due to Ca2+ dysregulation. Besides, the endoplasmic reticulum (ER) stress has an active role in the neurotoxic mechanisms that lead to these pathologies. Here, we analyzed whether the ER-mediated apoptotic pathway is involved in the toxic ...
Studies with in-vitro-cultured neurons treated with amyloid-beta (Abeta) peptides demonstrated neuronal loss by apoptosis that is due, at least in part, to the perturbation of intracellular Ca2+ homeostasis. In addition, it was shown that an endoplasmic reticulum (ER)-specific apoptotic pathway mediated by caspase-12, which is activated upon the perturbation of ER Ca2+ homeostasis, may contribute to Abeta toxic...
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 ind...
Financiadores do RCAAP | |||||||
![]() |
![]() |
![]() |
![]() |
![]() |
![]() |