D R Howlett

Summary

Affiliation: GlaxoSmithKline Research and Development
Country: USA

Publications

  1. ncbi Abeta deposition and related pathology in an APP x PS1 transgenic mouse model of Alzheimer's disease
    D R Howlett
    Neurology and GI CEDD, GlaxoSmithKline, Harlow, Essex, UK
    Histol Histopathol 23:67-76. 2008
  2. ncbi The pathology of APP transgenic mice: a model of Alzheimer's disease or simply overexpression of APP?
    D R Howlett
    Neurology CEDD, GlaxoSmithKline, Harlow, Essex, UK
    Histol Histopathol 24:83-100. 2009
  3. ncbi Ultrastructural and behavioural changes precede amyloid deposition in a transgenic model of Alzheimer's disease
    J C Richardson
    Neurology Centre of Excellence for Drug Discovery, GlaxoSmithKline, New Frontiers Science Park, Third Avenue, Harlow, Essex, CM19 5AW UK
    Neuroscience 122:213-28. 2003
  4. ncbi Characterisation of amyloid-induced inflammatory responses in the rat retina
    D R Howlett
    Neurosciences Centre of Excellence for Drug Discovery, GlaxoSmithKline R and D Limited, New Frontiers Science Park, Third Avenue, Harlow, Essex CM19 5AW, UK
    Exp Brain Res 214:185-97. 2011
  5. ncbi Identification of a novel aspartic protease (Asp 2) as beta-secretase
    I Hussain
    Department of Neurosciences, SmithKline Beecham Pharmaceuticals, Harlow, Essex, United Kingdom
    Mol Cell Neurosci 14:419-27. 1999
  6. ncbi Inhibition of fibril formation in beta-amyloid peptide by a novel series of benzofurans
    D R Howlett
    Department of Neuroscience, SmithKline Beecham Pharmaceuticals, New Frontiers Science Park North, Third Avenue, Harlow, Essex CM19 5AW, UK
    Biochem J 340:283-9. 1999

Detail Information

Publications6

  1. ncbi Abeta deposition and related pathology in an APP x PS1 transgenic mouse model of Alzheimer's disease
    D R Howlett
    Neurology and GI CEDD, GlaxoSmithKline, Harlow, Essex, UK
    Histol Histopathol 23:67-76. 2008
    ..TASTPM mice, therefore, exhibit a number of the pathological characteristics of disease progression in AD and may provide a means for assessment of novel therapeutic agents directed towards modifying or halting disease progression...
  2. ncbi The pathology of APP transgenic mice: a model of Alzheimer's disease or simply overexpression of APP?
    D R Howlett
    Neurology CEDD, GlaxoSmithKline, Harlow, Essex, UK
    Histol Histopathol 24:83-100. 2009
    ..Consequently, it is evident that APP transgenic mice exhibit, to some degree, many of the pathological features of AD...
  3. ncbi Ultrastructural and behavioural changes precede amyloid deposition in a transgenic model of Alzheimer's disease
    J C Richardson
    Neurology Centre of Excellence for Drug Discovery, GlaxoSmithKline, New Frontiers Science Park, Third Avenue, Harlow, Essex, CM19 5AW UK
    Neuroscience 122:213-28. 2003
    ....
  4. ncbi Characterisation of amyloid-induced inflammatory responses in the rat retina
    D R Howlett
    Neurosciences Centre of Excellence for Drug Discovery, GlaxoSmithKline R and D Limited, New Frontiers Science Park, Third Avenue, Harlow, Essex CM19 5AW, UK
    Exp Brain Res 214:185-97. 2011
    ....
  5. ncbi Identification of a novel aspartic protease (Asp 2) as beta-secretase
    I Hussain
    Department of Neurosciences, SmithKline Beecham Pharmaceuticals, Harlow, Essex, United Kingdom
    Mol Cell Neurosci 14:419-27. 1999
    ..Asp 2 localizes to the Golgi/endoplasmic reticulum in transfected cells and shows clear colocalization with APP in cells stably expressing the 751-amino-acid isoform of APP...
  6. ncbi Inhibition of fibril formation in beta-amyloid peptide by a novel series of benzofurans
    D R Howlett
    Department of Neuroscience, SmithKline Beecham Pharmaceuticals, New Frontiers Science Park North, Third Avenue, Harlow, Essex CM19 5AW, UK
    Biochem J 340:283-9. 1999
    ..Thus a specific recognition site might exist for benzofurans on beta-amyloid, binding to which seems to interfere with the ability of the peptide to form fibrils...