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OPA1 Controls Apoptotic Cristae Remodeling Independently from Mitochondrial Fusion
Mitochondria amplify activation of caspases during apoptosis by releasing cytochrome c and other cofactors. This is accompanied by fragmentation of the organelle and remodeling of the cristae. HereExpand
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The toxic Aβ oligomer and Alzheimer's disease: an emperor in need of clothes
The 'toxic Aβ oligomer' hypothesis has attracted considerable attention among Alzheimer's disease researchers as a way of resolving the lack of correlation between deposited amyloid-β (Aβ) in amyloidExpand
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Mitochondrial Rhomboid PARL Regulates Cytochrome c Release during Apoptosis via OPA1-Dependent Cristae Remodeling
Rhomboids, evolutionarily conserved integral membrane proteases, participate in crucial signaling pathways. Presenilin-associated rhomboid-like (PARL) is an inner mitochondrial membrane rhomboid ofExpand
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The amyloid cascade hypothesis for Alzheimer's disease: an appraisal for the development of therapeutics
The amyloid cascade hypothesis, which posits that the deposition of the amyloid-β peptide in the brain is a central event in Alzheimer's disease pathology, has dominated research for the past twentyExpand
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A presenilin-1-dependent γ-secretase-like protease mediates release of Notch intracellular domain
Signalling through the receptor protein Notch, which is involved in crucial cell-fate decisions during development, requires ligand-induced cleavage of Notch. This cleavage occurs within theExpand
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Deficiency of presenilin-1 inhibits the normal cleavage of amyloid precursor protein
Point mutations in the presenilin-1 gene (PS1) are a major cause of familial Alzheimer's disease. They result in a selective increase in the production of the amyloidogenic peptide amyloid-β(1–42) byExpand
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Presenilins Form ER Ca2+ Leak Channels, a Function Disrupted by Familial Alzheimer's Disease-Linked Mutations
Alzheimer's disease (AD) is a progressive and irreversible neurodegenerative disorder. Mutations in presenilins 1 and 2 (PS1 and PS2) account for approximately 40% of familial AD (FAD) cases. FADExpand
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Presenilin clinical mutations can affect γ‐secretase activity by different mechanisms
Mutations in human presenilin (PS) genes cause aggressive forms of familial Alzheimer's disease. Presenilins are polytopic proteins that harbour the catalytic site of the γ‐secretase complex andExpand
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The Cellular Phase of Alzheimer’s Disease
The amyloid hypothesis for Alzheimer's disease (AD) posits a neuron-centric, linear cascade initiated by Aβ and leading to dementia. This direct causality is incompatible with clinical observations.Expand
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Destabilization of β-catenin by mutations in presenilin-1 potentiates neuronal apoptosis
Mutations of the presenilin-1 gene are a major cause of familial early-onset Alzheimer's disease. Presenilin-1 can associate with members of the catenin family of signalling proteins, but theExpand
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