Amyloid beta-Protein Precursor

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  Subject Areas on Research

  • A molecular genetic study of intracerebral hemorrhage. 
  • A neuronal model of Alzheimer's disease: an insight into the mechanisms of oxidative stress-mediated mitochondrial injury. 
  • A novel species-specific RNA related to alternatively spliced amyloid precursor protein mRNAs. 
  • A prior feature SVM-MRF based method for mouse brain segmentation. 
  • ADAM9 inhibition increases membrane activity of ADAM10 and controls α-secretase processing of amyloid precursor protein. 
  • AMY plaques in familial AD: comparison with sporadic Alzheimer's disease. 
  • APOE-mimetic peptides reduce behavioral deficits, plaques and tangles in Alzheimer's disease transgenics. 
  • APP717, APP693, and PRIP gene mutations are rare in Alzheimer disease. 
  • Absence of A673T amyloid-β precursor protein variant in Alzheimer's disease and other neurological diseases. 
  • Age-Dependent Effects of apoE Reduction Using Antisense Oligonucleotides in a Model of β-amyloidosis. 
  • Altered genetic response to beta-adrenergic receptor activation in late passage C6 glioma cells. 
  • Altered neuronal gene expression in brain regions differentially affected by Alzheimer's disease: a reference data set. 
  • Alzheimer's disease and apolipoprotein E-4 allele in an Amish population. 
  • Alzheimer's disease and possible gene interaction. 
  • Amyloid precursor protein 96-110 and beta-amyloid 1-42 elicit developmental anomalies in sea urchin embryos and larvae that are alleviated by neurotransmitter analogs for acetylcholine, serotonin and cannabinoids. 
  • Amyloid precursor protein and amyloid beta-peptide bind to ATP synthase and regulate its activity at the surface of neural cells. 
  • Amyloid precursor protein processing and Alzheimer's disease. 
  • Amyloid-beta-protein isoforms in brain of subjects with PS1-linked, beta APP-linked and sporadic Alzheimer disease. 
  • Apolipoprotein E affects the rate of Alzheimer disease expression: beta-amyloid burden is a secondary consequence dependent on APOE genotype and duration of disease. 
  • Arginine deprivation and immune suppression in a mouse model of Alzheimer's disease. 
  • Assessment of the genetic variance of late-onset Alzheimer's disease. 
  • Avid binding of beta A amyloid peptide to its own precursor. 
  • Blocking the apoE/Aβ interaction ameliorates Aβ-related pathology in APOE ε2 and ε4 targeted replacement Alzheimer model mice. 
  • CD36 initiates the secretory phenotype during the establishment of cellular senescence. 
  • Caspase activation and amyloid precursor protein cleavage in rat ocular hypertension. 
  • Clinical comparison of Alzheimer's disease in pedigrees with the codon 717 Val-->Ile mutation in the amyloid precursor protein gene. 
  • Decoy mRNAs reduce beta-amyloid precursor protein mRNA in neuronal cells. 
  • Defective phorbol ester-stimulated secretion of beta-amyloid precursor protein from Alzheimer's disease fibroblasts. 
  • Differential roles of Aβ processing in hypoxia-induced axonal damage. 
  • Distribution of amyloid precursor protein and amyloid-beta in ocular hypertensive C57BL/6 mouse eyes. 
  • Diverse inflammatory responses in transgenic mouse models of Alzheimer's disease and the effect of immunotherapy on these responses. 
  • Does epileptiform activity contribute to cognitive impairment in Alzheimer's disease? 
  • Early induction of oxidative stress in mouse model of Alzheimer disease with reduced mitochondrial superoxide dismutase activity. 
  • Ectopic white matter neurons, a developmental abnormality that may be caused by the PSEN1 S169L mutation in a case of familial AD with myoclonus and seizures. 
  • Endocytic disturbances distinguish among subtypes of Alzheimer's disease and related disorders. 
  • Familial and sporadic Alzheimer's disease: neuropathology cannot exclude a final common pathway. 
  • Focusing on IL-1-promotion of beta-amyloid precursor protein synthesis as an early event in Alzheimer's disease. 
  • Gene identification in Alzheimer's disease. 
  • Genes and recent developments in the epidemiology of Alzheimer's disease and related dementia. 
  • Genetic evidence for a novel familial Alzheimer's disease locus on chromosome 14. 
  • Genetic studies in Alzheimer's disease with an NACP/alpha-synuclein polymorphism. 
  • Genome-wide analysis of miRNA signature in the APPswe/PS1ΔE9 mouse model of alzheimer's disease. 
  • Genome-wide, high-content siRNA screening identifies the Alzheimer's genetic risk factor FERMT2 as a major modulator of APP metabolism. 
  • Human APOE isoform-dependent effects on brain beta-amyloid levels in PDAPP transgenic mice. 
  • Human apolipoprotein E4 alters the amyloid-beta 40:42 ratio and promotes the formation of cerebral amyloid angiopathy in an amyloid precursor protein transgenic model. 
  • Human apolipoprotein E4 worsens acute axonal pathology but not amyloid-β immunoreactivity after traumatic brain injury in 3xTG-AD mice. 
  • Iatrogenic Alzheimer Disease? Amyloid-β Protein Transmission Between Humans. 
  • Identification of candidate substrates for ectodomain shedding by the metalloprotease-disintegrin ADAM8. 
  • Increasing amyloid peptide precursor production and its impact on Alzheimer's disease. 
  • Inhibition of c-Jun kinase provides neuroprotection in a model of Alzheimer's disease. 
  • Inhibitors of protein disulfide isomerase suppress apoptosis induced by misfolded proteins. 
  • Interleukin 1 regulates synthesis of amyloid beta-protein precursor mRNA in human endothelial cells. 
  • Isolation and expression of multiple forms of beta amyloid protein precursor cDNAs. 
  • Large quantities of Abeta peptide are constitutively released during amyloid precursor protein metabolism in vivo and in vitro. 
  • Lewy body and Alzheimer pathology in a family with the amyloid-beta precursor protein APP717 gene mutation. 
  • Lithium treatment of APPSwDI/NOS2-/- mice leads to reduced hyperphosphorylated tau, increased amyloid deposition and altered inflammatory phenotype. 
  • Loss of tau elicits axonal degeneration in a mouse model of Alzheimer's disease. 
  • Melatonin increases survival and inhibits oxidative and amyloid pathology in a transgenic model of Alzheimer's disease. 
  • Microglial oxyradical production: causes and consequences. 
  • Multiple forms of beta-amyloid peptide precursor RNAs in a single cell type. 
  • Murine versus human apolipoprotein E4: differential facilitation of and co-localization in cerebral amyloid angiopathy and amyloid plaques in APP transgenic mouse models. 
  • New Insights to Clathrin and Adaptor Protein 2 for the Design and Development of Therapeutic Strategies. 
  • Nicotinic neuronal acetylcholine receptor alpha-3 subunit transcription in normal and myasthenic thymus. 
  • Novel polymorphism in the A4 region of the amyloid precursor protein gene in a patient without Alzheimer's disease. 
  • PDAPP; YFP double transgenic mice: a tool to study amyloid-beta associated changes in axonal, dendritic, and synaptic structures. 
  • Presenilin-1 mutations in Alzheimer's disease. 
  • Quantitative measurement of alternatively spliced amyloid precursor protein mRNA expression in Alzheimer's disease and normal brain by S1 nuclease protection analysis. 
  • Quantitative measurement of postural sway in mouse models of human neurodegenerative disease. 
  • RFLP analysis for APP 717 mutations associated with Alzheimer's disease. 
  • Rarity of the Alzheimer disease-protective APP A673T variant in the United States. 
  • Re: Axonal injury in head injuries with very short survival. 
  • Reducing cerebral microvascular amyloid-beta protein deposition diminishes regional neuroinflammation in vasculotropic mutant amyloid precursor protein transgenic mice. 
  • Relative abundance of Alzheimer A beta amyloid peptide variants in Alzheimer disease and normal aging. 
  • Release of amino-terminal fragments from amyloid precursor protein reporter and mutated derivatives in cultured cells. 
  • Schizophrenia scepticism. 
  • Segregation of a missense mutation in the amyloid precursor protein gene with familial Alzheimer's disease. 
  • Selectivity, cocrystal structures, and neuroprotective properties of leucettines, a family of protein kinase inhibitors derived from the marine sponge alkaloid leucettamine B. 
  • Sequestration of amyloid beta-peptide. 
  • Synergistic Interactions between Abeta, tau, and alpha-synuclein: acceleration of neuropathology and cognitive decline. 
  • Tau Protein Mediates APP Intracellular Domain (AICD)-Induced Alzheimer's-Like Pathological Features in Mice. 
  • The ADAM10 prodomain is a specific inhibitor of ADAM10 proteolytic activity and inhibits cellular shedding events. 
  • The Alzheimer diseases. 
  • The apolipoprotein-E-mimetic COG112 protects amyloid precursor protein intracellular domain-overexpressing animals from Alzheimer's disease-like pathological features. 
  • The effects of NOS2 gene deletion on mice expressing mutated human AbetaPP. 
  • The genetics of dementia in late life. 
  • The low density lipoprotein receptor regulates the level of central nervous system human and murine apolipoprotein E but does not modify amyloid plaque pathology in PDAPP mice. 
  • Thymocytes and cultured thymic epithelial cells express transcripts encoding alpha-3, alpha-5 and beta-4 subunits of neuronal nicotinic acetylcholine receptors: preferential transcription of the alpha-3 and beta-4 genes by immature CD4 + 8 + thymocytes. 
  • TrkB activation by 7, 8-dihydroxyflavone increases synapse AMPA subunits and ameliorates spatial memory deficits in a mouse model of Alzheimer's disease. 
  • Tumor necrosis factor alpha and Fas receptor contribute to cognitive deficits independent of cell death after concussive traumatic brain injury in mice. 
  • Vascular amyloid alters astrocytic water and potassium channels in mouse models and humans with Alzheimer's disease. 
  • [Investigation of neuroprotective activity of apolipoprotein E peptide mimetic Cog1410 in transgenic lines of Drosophila melanogaster]. 
  • [Studying pathogenesis of Alzheimer's disease in a Drosophila melanogaster model: human APP overexpression in the brain of transgenic flies leads to deficit of the synaptic protein synaptotagmin]. 
  • mNos2 deletion and human NOS2 replacement in Alzheimer disease models. 
  • p53-dependent control of transactivation of the Pen2 promoter by presenilins.