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BACE knockout mice are healthy despite lacking the primary beta-secretase activity in brain: Implications for Alzheimer’s disease therapeutics

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β-Secretase Protein and Activity Are Increased in the Neocortex in Alzheimer Disease

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APPSW Transgenic Mice Develop Age-related Aβ Deposits and Neuropil Abnormalities, but no Neuronal Loss in CA1

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Maturation and Endosomal Targeting of β-Site Amyloid Precursor Protein-cleaving Enzyme

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Oxidative stress increases expression and activity of BACE in NT2 neurons

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Compartmentalization of β-secretase (Asp2) into low-buoyant density, noncaveolar lipid rafts

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Demonstration by FRET of BACE interaction with the amyloid precursor protein at the cell surface and in early endosomes

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Maturation and Pro-peptide Cleavage of β-Secretase

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Region‐specific reduction of Aβ‐degrading endopeptidase, neprilysin, in mouse hippocampus upon aging

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Astrocytic expression of the Alzheimer's disease β‐secretase (BACE1) is stimulus‐dependent

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Proteolytic Activation of Recombinant Pro-memapsin 2 (Pro-β-secretase) Studied with New Fluorogenic Substrates

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The Pro Domain of β-Secretase Does Not Confer Strict Zymogen-like Properties but Does Assist Proper Folding of the Protease Domain

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Expression of human β‐secretase in the mouse brain increases the steady‐state level of β‐amyloid

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The beta APP717 Alzheimer mutation increases the percentage of plasma amyloid-beta protein ending at A beta 42(43)

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Neuronal and glial β‐secretase (BACE) protein expression in transgenic Tg2576 mice with amyloid plaque pathology

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β-Site APP Cleaving Enzyme mRNA Expression in APP Transgenic Mice

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Three novel alternatively spliced isoforms of the human beta-site amyloid precursor protein cleaving enzyme (BACE) and their effect on amyloid beta-peptide production

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Developmental Regulation of Presenilin mRNA Expression Parallels Notch Expression

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Identification of Phospholipid Scramblase 1 as a Novel Interacting Molecule with β-Secretase (β-Site Amyloid Precursor Protein (APP) Cleaving Enzyme (BACE))

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Localization of β-Secretase Memapsin 2 in the Brain of Alzheimer's Patients and Normal Aged Controls

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Endoproteolysis of औ-Secretase (औ-Site Amyloid Precursor Protein-cleaving Enzyme) within Its Catalytic Domain

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Age-related changes in the localization of presenilin-1 in cynomolgus monkey brain

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BACE1 interacts with nicastrin

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Alzheimer's Disease and the Amyloid-β Peptide

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A Diet Enriched with the Omega-3 Fatty Acid Docosahexaenoic Acid Reduces Amyloid Burden in an Aged Alzheimer Mouse Model

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Hypoxia facilitates Alzheimer's disease pathogenesis by up-regulating <i>BACE1</i> gene expression

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The Alzheimer's disease Beta-secretase enzyme, BACE1

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Inhibition of GSK3β-mediated BACE1 expression reduces Alzheimer-associated phenotypes

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Probing the biology of Alzheimer’s disease in mice

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Nonsteroidal anti-inflammatory drugs repress β-secretase gene promoter activity by the activation of PPARγ

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Current Pharmacotherapy for Alzheimer's Disease

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Autophagic vacuoles are enriched in amyloid precursor protein-secretase activities: implications for β-amyloid peptide over-production and localization in Alzheimer’s disease

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The Role of Amyloid Precursor Protein Processing by BACE1, the β-Secretase, in Alzheimer Disease Pathophysiology*

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Synaptic Changes in Alzheimer's Disease

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The mitochondrial impairment, oxidative stress and neurodegeneration connection: reality or just an attractive hypothesis?

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Docosahexaenoic Acid and the Aging Brain

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Deletion of the Prostaglandin E2EP2 Receptor Reduces Oxidative Damage and Amyloid Burden in a Model of Alzheimer's Disease

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Updates in Alzheimer's disease: from basic research to diagnosis and therapies

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Soy isoflavones attenuate oxidative stress and improve parameters related to aging and Alzheimer’s disease in C57BL/6J mice treated with d-galactose

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Nonsteroidal anti-inflammatory drugs lower Aβ42 and change presenilin 1 conformation

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Transcriptional and translational regulation of BACE1 expression—Implications for Alzheimer's disease

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Genetic deletion of BACE1 in mice affects remyelination of sciatic nerves

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Mechanisms of Melatonin in Alleviating Alzheimer’s Disease

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Molecular mechanisms of neuropathological changes in Alzheimer’s disease: a review

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Palmitoylation of Amyloid Precursor Protein Regulates Amyloidogenic Processing in Lipid Rafts

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Aging‐related increase in oxidative stress correlates with developmental pattern of beta‐secretase activity and beta‐amyloid plaque formation in transgenic Tg2576 mice with Alzheimer‐like pathology

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Behavioral phenotypes of amyloid‐based genetically modified mouse models of Alzheimer's disease

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Lack of Genetic Associations of PPAR-γ and PGC-1α with Alzheimer's Disease and Parkinson's Disease with Dementia

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Expression and functional profiling of neprilysin, insulin‐degrading enzyme, and endothelin‐converting enzyme in prospectively studied elderly and Alzheimer’s brain

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Nonhuman Primate Models of Alzheimer-Like Cerebral Proteopathy

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BACE1 is at the crossroad of a toxic vicious cycle involving cellular stress and β-amyloid production in Alzheimer’s disease

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BACE Is Degraded via the Lysosomal Pathway

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Age-dependent decline of neprilysin in Alzheimer's disease and normal brain: Inverse correlation with Aβ levels

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Alzheimer's disease β‐secretase BACE1 is not a neuron‐specific enzyme

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Systemic Mitochondrial Dysfunction and the Etiology of Alzheimer's Disease and Down Syndrome Dementia

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BACE2, as a novel APP θ‐secretase, is not responsible for the pathogenesis of Alzheimer's disease in Down syndrome

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Deficiency of Neuronal p38α MAPK Attenuates Amyloid Pathology in Alzheimer Disease Mouse and Cell Models through Facilitating Lysosomal Degradation of BACE1*

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Loss of Cathepsin B and L Leads to Lysosomal Dysfunction, NPC-Like Cholesterol Sequestration and Accumulation of the Key Alzheimer's Proteins

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A TrkA-to-p75NTR molecular switch activates amyloid β-peptide generation during aging

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