Intracellular amyloid-beta in Alzheimer's disease.

By F. LaFerla, K. Green, S. Oddo. Nature Reviews Neuroscience, 2007

838 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/fa350d4a1b2c51da5d7d6ca56ed8582cc19c1888

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Citations in the corpus

• Autophagy, amyloidogenesis and Alzheimer disease (2007, unknown): “In its pathologic oligomeric state, A exerts a range of cytotoxic actions considered important to the evolution of neurodegeneration in AD (Selkoe, 2001; Watson et al., 2005; Small et al., 2001; Laferla et al., 2007; Lee et al., 2006).”
• The autophagy-related protein beclin 1 shows reduced expression in early Alzheimer disease and regulates amyloid beta accumulation in mice. (2008, background): “Abeta deposition is associated with neuropil changes, but not with overt neuronal loss in the human amyloid precursor protein V717F (PDAPP) transgenic mouse.”
• Impaired mitochondrial dynamics and abnormal interaction of amyloid beta with mitochondrial protein Drp1 in neurons from patients with Alzheimer's disease: implications for neuronal damage. (2011, background): “A reduction in the clearance of Ab or the overproduction of Ab may lead to an accumulation of Ab in subcellular compartments of neuron, including mitochondria, endoplasmic reticulum, lysosomes and multiple vesicle bodies, and may impair functions of subcellular organelles and damage neurons (8,16).”
• Amyloid beta, mitochondrial dysfunction and synaptic damage: implications for cognitive decline in aging and Alzheimer's disease. (2008, background): “function [13], and promotes cellular changes.”
• Drosophila orthologues to human disease genes: an update on progress. (2008, background): “The hallmark lesion in Alzheimer’s disease is characterized by the formation of Ab peptide‐ containing amyloid plaques in brain [reviewed in (18, 19)].”
• Oxidative Stress, Synaptic Dysfunction, and Alzheimer’s Disease (2017, background): “While cleavage of A PP at the plasma membrane by the α-secretase occurs without formation of pathologic amyloid-β (A ) peptides, cleavage with - and -secretases leads to the release in the extracellular space of A peptides with 40 or 42 residues where A 42 is more prone to aggregation and is the maj”
• Impaired mitochondrial biogenesis, defective axonal transport of mitochondria, abnormal mitochondrial dynamics and synaptic degeneration in a mouse model of Alzheimer's disease. (2011, background): “The pathological hallmarks of AD are amyloid plaques and neurofibrillary tangles (1,2).”
• Amyloid Precursor Protein Processing and Alzheimer’s Disease (2011, background): “…had suggested that significant amounts of APP were processed to Aβ intracellularly (Greenfield et al. 1999), and evidence provides support for BACE1 in the TGN (Huse et al. 2002) and for intracellular Aβ accumulation in neurons from patients with early AD (Gouras et al 2000; LaFerla et al 2007).”