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B. Maloney [41]Bryan Maloney [1]Bridget Maloney [1]
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Bryan Maloney
Indiana University Purdue University, Indianapolis
  1.  3
    Lessons From a BACE1 Inhibitor Trial: Off-Site but Not Off Base.D. K. Lahiri, B. Maloney, J. M. Long & N. H. Greig - 2014 - Alzheimers Dement 10:S411-9.
    Alzheimer's disease is characterized by formation of neuritic plaque primarily composed of a small filamentous protein called amyloid-beta peptide . The rate-limiting step in the production of Abeta is the processing of Abeta precursor protein by beta-site APP-cleaving enzyme . Hence, BACE1 activity plausibly plays a rate-limiting role in the generation of potentially toxic Abeta within brain and the development of AD, thereby making it an interesting drug target. A phase II trial of the promising LY2886721 inhibitor of BACE1 was (...)
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  2.  3
    Early-Emerging Cognitive Vulnerability to Depression and the Serotonin Transporter Promoter Region Polymorphism.E. P. Hayden, L. R. Dougherty, B. Maloney, T. M. Olino, H. Sheikh, C. E. Durbin, J. I. Nurnberger Jr, D. K. Lahiri & D. N. Klein - 2008 - J Affect Disord 107:227-30.
    BACKGROUND: Serotonin transporter promoter genotype appears to increase risk for depression in the context of stressful life events. However, the effects of this genotype on measures of stress sensitivity are poorly understood. Therefore, this study examined whether 5-HTTLPR genotype was associated with negative information processing biases in early childhood. METHOD: Thirty-nine unselected seven-year-old children completed a negative mood induction procedure and a Self-Referent Encoding Task designed to measure positive and negative schematic processing. Children were also genotyped for the 5-HTTLPR gene. (...)
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  3.  16
    NF-B Mediates Amyloid Beta Peptide-Stimulated Activity of the Human Apolipoprotein E Gene Promoter in Human Astroglial Cells.Y. Du, X. Chen, X. Wei, K. R. Bales, D. T. Berg, S. M. Paul, M. R. Farlow, B. Maloney, Y. W. Ge & D. K. Lahiri - 2005 - Brain Res Mol Brain Res 136:177-88.
    The apolipoprotein E gene plays an important role in the pathogenesis of Alzheimer's disease , and amyloid plaque comprised mostly of the amyloid-beta peptide ) is one of the major hallmarks of AD. However, the relationship between these two important molecules is poorly understood. We examined how A treatment affects APOE expression in cultured cells and tested the role of the transcription factor NF-B in APOE gene regulation. To delineate NF-B's role, we have characterized a 1098 nucleotide segment containing the (...)
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  4.  12
    The Experimental Alzheimer's Disease Drug Posiphen [-Phenserine] Lowers Amyloid-Beta Peptide Levels in Cell Culture and Mice.D. K. Lahiri, D. Chen, B. Maloney, H. W. Holloway, Q. S. Yu, T. Utsuki, T. Giordano, K. Sambamurti & N. H. Greig - 2007 - J Pharmacol Exp Ther 320:386-96.
    Major characteristics of Alzheimer's disease are synaptic loss, cholinergic dysfunction, and abnormal protein depositions in the brain. The amyloid beta-peptide , a proteolytic fragment of amyloid beta precursor protein , aggregates to form neuritic plaques and has a causative role in AD. A present focus of AD research is to develop safe Abeta-lowering drugs. A selective acetylcholinesterase inhibitor, phenserine, in current human trials lowers both APP and Abeta. Phenserine is dose-limited in animals by its cholinergic actions; its cholinergically inactive enantiomer, (...)
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  5.  12
    Alzheimer's Disease -Like Pathology in Aged Monkeys After Infantile Exposure to Environmental Metal Lead : Evidence for a Developmental Origin and Environmental Link for AD.J. Wu, M. R. Basha, B. Brock, D. P. Cox, F. Cardozo-Pelaez, C. A. McPherson, J. Harry, D. C. Rice, B. Maloney, D. Chen, D. K. Lahiri & N. H. Zawia - 2008 - J Neurosci 28:3-9.
    The sporadic nature of Alzheimer's disease argues for an environmental link that may drive AD pathogenesis; however, the triggering factors and the period of their action are unknown. Recent studies in rodents have shown that exposure to lead during brain development predetermined the expression and regulation of the amyloid precursor protein and its amyloidogenic beta-amyloid product in old age. Here, we report that the expression of AD-related genes [APP, BACE1 ] as well as their transcriptional regulator were elevated in aged (...)
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  6.  11
    Lifespan Profiles of Alzheimer's Disease-Associated Genes and Products in Monkeys and Mice.R. Dosunmu, J. Wu, L. Adwan, B. Maloney, M. R. Basha, C. A. McPherson, G. J. Harry, D. C. Rice, N. H. Zawia & D. K. Lahiri - 2009 - J Alzheimers Dis 18:211-30.
    Alzheimer's disease is characterized by plaques of amyloid-beta peptide, cleaved from amyloid-beta protein precursor . Our hypothesis is that lifespan profiles of AD-associated mRNA and protein levels in monkeys would differ from mice and that differential lifespan expression profiles would be useful to understand human AD pathogenesis. We compared profiles of AbetaPP mRNA, AbetaPP protein, and Abeta levels in rodents and primates. We also tracked a transcriptional regulator of the AbetaPP gene, specificity protein 1 , and the beta amyloid precursor (...)
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  7.  8
    Functional Activity of the Novel Alzheimer's Amyloid Beta-Peptide Interacting Domain in the APP and BACE1 Promoter Sequences and Implications in Activating Apoptotic Genes and in Amyloidogenesis.J. A. Bailey, B. Maloney, Y. W. Ge & D. K. Lahiri - 2011 - Gene 488:13-22.
    Amyloid-beta peptide plaque in the brain is the primary diagnostic criterion of Alzheimer's disease . The physiological role of Abeta are poorly understood. We have previously determined an Abeta interacting domain in the promoters of AD-associated genes . This AbetaID interacts in a DNA sequence-specific manner with Abeta. We now demonstrate novel Abeta activity as a possible transcription factor. Herein, we detected Abeta-chromatin interaction in cell culture by ChIP assay. We observed that human neuroblastoma cells treated with FITC conjugated Abeta1-40 (...)
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  8.  5
    Functional Characterization of Three Single-Nucleotide Polymorphisms Present in the Human APOE Promoter Sequence: Differential Effects in Neuronal Cells and on DNA-Protein Interactions.B. Maloney, Y. W. Ge, R. C. Petersen, J. Hardy, J. T. Rogers, J. Perez-Tur & D. K. Lahiri - 2010 - Am J Med Genet B Neuropsychiatr Genet 153:185-201.
    Variations in levels of apolipoprotein E have been tied to the risk and progression of Alzheimer's disease . Our group has previously compared and contrasted the promoters of the mouse and human ApoE gene promoter sequences and found notable similarities and significant differences that suggest the importance of the APOE promoter's role in the human disease. We examine here three specific single-nucleotide polymorphisms within the human APOE promoter region, specifically at -491 , -427 , and at -219 upstream from the (...)
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  9.  5
    Transcriptional Regulation of Beta-Secretase by P25/Cdk5 Leads to Enhanced Amyloidogenic Processing.Y. Wen, W. H. Yu, B. Maloney, J. Bailey, J. Ma, I. Marie, T. Maurin, L. Wang, H. Figueroa, M. Herman, P. Krishnamurthy, L. Liu, E. Planel, L. F. Lau, D. K. Lahiri & K. Duff - 2008 - Neuron 57:680-90.
    Cyclin-dependent kinase 5 has been implicated in Alzheimer's disease pathogenesis. Here, we demonstrate that overexpression of p25, an activator of cdk5, led to increased levels of BACE1 mRNA and protein in vitro and in vivo. A p25/cdk5 responsive region containing multiple sites for signal transducer and activator of transcription was identified in the BACE1 promoter. STAT3 interacts with the BACE1 promoter, and p25-overexpressing mice had elevated levels of pSTAT3 and BACE1, whereas cdk5-deficient mice had reduced levels. Furthermore, mice with a (...)
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  10.  4
    Exposure to Lead and the Developmental Origin of Oxidative DNA Damage in the Aging Brain.C. M. Bolin, R. Basha, D. Cox, N. H. Zawia, B. Maloney, D. K. Lahiri & F. Cardozo-Pelaez - 2006 - Faseb J 20:788-90.
    Oxidative damage to DNA has been associated with neurodegenerative diseases. Developmental exposure to lead has been shown to elevate the Alzheimer's disease related beta-amyloid peptide , which is known to generate reactive oxygen species in the aging brain. This study measures the lifetime cerebral 8-hydroxy-2'-deoxyguanosine levels and the activity of the DNA repair enzyme 8-oxoguanine DNA glycosylase in rats developmentally exposed to Pb. Oxo8dG was transiently modulated early in life , but was later elevated 20 months after exposure to Pb (...)
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  11.  2
    Taking Down the Unindicted Co-Conspirators of Amyloid Beta-Peptide-Mediated Neuronal Death: Shared Gene Regulation of BACE1 and APP Genes Interacting with CREB, Fe65 and YY1 Transcription Factors. [REVIEW]D. K. Lahiri, Y. W. Ge, J. T. Rogers, K. Sambamurti, N. H. Greig & B. Maloney - 2006 - Curr Alzheimer Res 3:475-83.
    Major hallmarks of Alzheimer's disease include brain deposition of the amyloid-beta peptide , which is proteolytically cleaved from a large Abeta precursor protein by beta and gamma- secretases. A transmembrane aspartyl protease, beta-APP cleaving enzyme , has been recognized as the beta-secretase. We review the structure and function of the BACE1 protein, and of 4129 bp of the 5'-flanking region sequence of the BACE1 gene and its interaction with various transcription factors involved in cell signaling. The promoter region and 5'-untranslated (...)
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  12.  1
    Temperamental Fearfulness in Childhood and the Serotonin Transporter Promoter Region Polymorphism: A Multimethod Association Study.E. P. Hayden, L. R. Dougherty, B. Maloney, C. Emily Durbin, T. M. Olino, J. I. Nurnberger Jr, D. K. Lahiri & D. N. Klein - 2007 - Psychiatr Genet 17:135-42.
    OBJECTIVES: Early-emerging, temperamental differences in fear-related traits may be a heritable vulnerability factor for anxiety disorders. Previous research indicates that the serotonin transporter promoter region polymorphism is a candidate gene for such traits. METHODS: Associations between 5-HTTLPR genotype and indices of fearful child temperament, derived from maternal report and standardized laboratory observations, were examined in a community sample of 95 preschool-aged children. RESULTS: Children with one or more long alleles of the 5-HTTLPR gene were rated as significantly more nervous during (...)
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  13.  1
    PuF, an Antimetastatic and Developmental Signaling Protein, Interacts with the Alzheimer's Amyloid-Beta Precursor Protein Via a Tissue-Specific Proximal Regulatory Element.D. K. Lahiri, B. Maloney, J. T. Rogers & Y. W. Ge - 2013 - Bmc Genomics 14:68.
    BACKGROUND: Alzheimer's disease is intimately tied to amyloid-beta peptide. Extraneuronal brain plaques consisting primarily of Abeta aggregates are a hallmark of AD. Intraneuronal Abeta subunits are strongly implicated in disease progression. Protein sequence mutations of the Abeta precursor protein account for a small proportion of AD cases, suggesting that regulation of the associated gene may play a more important role in AD etiology. The APP promoter possesses a novel 30 nucleotide sequence, or "proximal regulatory element" , at -76/-47, from the (...)
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  14. Co-Localization and Distribution of Cerebral APP and SP1 and its Relationship to Amyloidogenesis.B. Brock, R. Basha, K. DiPalma, A. Anderson, G. J. Harry, D. C. Rice, B. Maloney, D. K. Lahiri & N. H. Zawia - 2008 - J Alzheimers Dis 13:71-80.
    Alzheimer's disease is characterized by amyloid-beta peptide -loaded plaques in the brain. Abeta is a cleavage fragment of amyloid-beta protein precursor and over production of APP may lead to amyloidogenesis. The regulatory region of the APP gene contains consensus sites recognized by the transcription factor, specificity protein 1 , which has been shown to be required for the regulation of APP and Abeta. To understand the role of SP1 in APP biogenesis, herein we have characterized the relative distribution and localization (...)
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  15. Autism, Alzheimer Disease, and Fragile X: APP, FMRP, and mGluR5 Are Molecular Links.D. K. Sokol, B. Maloney, J. M. Long, B. Ray & D. K. Lahiri - 2011 - Neurology 76:1344-52.
    The present review highlights an association between autism, Alzheimer disease , and fragile X syndrome . We propose a conceptual framework involving the amyloid-beta peptide , Abeta precursor protein , and fragile X mental retardation protein based on experimental evidence. The anabolic effect of the secreted alpha form of the amyloid-beta precursor protein may contribute to the state of brain overgrowth implicated in autism and FXS. Our previous report demonstrated that higher plasma sAPPalpha levels associate with more severe symptoms of (...)
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