Henri J Huttunen

Summary

Affiliation: Harvard University
Country: USA

Publications

  1. pmc Knockdown of ACAT-1 reduces amyloidogenic processing of APP
    Henri J Huttunen
    Neurobiology of Disease Laboratory, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, United States
    FEBS Lett 581:1688-92. 2007
  2. pmc Inhibition of acyl-coenzyme A: cholesterol acyl transferase modulates amyloid precursor protein trafficking in the early secretory pathway
    Henri J Huttunen
    Neurobiology of Disease Laboratory, Genetics and Aging Research Unit, Massachusetts General Hospital, Harvard Medical School, 114 16th Street, Charlestown, MA 02129, USA
    FASEB J 23:3819-28. 2009
  3. pmc The acyl-coenzyme A: cholesterol acyltransferase inhibitor CI-1011 reverses diffuse brain amyloid pathology in aged amyloid precursor protein transgenic mice
    Henri J Huttunen
    Neurobiology of Disease Laboratory, Genetics and Aging Research Unit, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA
    J Neuropathol Exp Neurol 69:777-88. 2010
  4. pmc Novel N-terminal cleavage of APP precludes Abeta generation in ACAT-defective AC29 cells
    Henri J Huttunen
    Neurobiology of Disease Laboratory, Genetics, and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease MIND and Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA
    J Mol Neurosci 37:6-15. 2009
  5. ncbi request reprint HtrA2 regulates beta-amyloid precursor protein (APP) metabolism through endoplasmic reticulum-associated degradation
    Henri J Huttunen
    Neurobiology of Disease Laboratory, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA
    J Biol Chem 282:28285-95. 2007
  6. pmc ACAT as a drug target for Alzheimer's disease
    Henri J Huttunen
    Neurobiology of Disease Laboratory, Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School, Charlestown, Mass 02129, USA
    Neurodegener Dis 5:212-4. 2008
  7. ncbi request reprint The ACAT inhibitor CP-113,818 markedly reduces amyloid pathology in a mouse model of Alzheimer's disease
    Birgit Hutter-Paier
    JSW Research Forschungslabor GmbH, Institute of Experimental Pharmacology, Rankengasse 28, 8020 Graz, Austria
    Neuron 44:227-38. 2004

Collaborators

Detail Information

Publications7

  1. pmc Knockdown of ACAT-1 reduces amyloidogenic processing of APP
    Henri J Huttunen
    Neurobiology of Disease Laboratory, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, United States
    FEBS Lett 581:1688-92. 2007
    ..This correlated with reduced proteolytic processing of APP and 40% decrease in Abeta secretion. These data show that even a modest decrease in ACAT activity can have robust suppressive effects on Abeta generation...
  2. pmc Inhibition of acyl-coenzyme A: cholesterol acyl transferase modulates amyloid precursor protein trafficking in the early secretory pathway
    Henri J Huttunen
    Neurobiology of Disease Laboratory, Genetics and Aging Research Unit, Massachusetts General Hospital, Harvard Medical School, 114 16th Street, Charlestown, MA 02129, USA
    FASEB J 23:3819-28. 2009
    ..Our results identify a novel ACAT-dependent mechanism that regulates secretory trafficking of APP, likely contributing to decreased Abeta generation in vivo...
  3. pmc The acyl-coenzyme A: cholesterol acyltransferase inhibitor CI-1011 reverses diffuse brain amyloid pathology in aged amyloid precursor protein transgenic mice
    Henri J Huttunen
    Neurobiology of Disease Laboratory, Genetics and Aging Research Unit, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA
    J Neuropathol Exp Neurol 69:777-88. 2010
    ..Collectively, these data suggest that CI-1011 treatment reduces amyloid burden in human APP mice by limiting generation and increasing clearance of diffusible Abeta...
  4. pmc Novel N-terminal cleavage of APP precludes Abeta generation in ACAT-defective AC29 cells
    Henri J Huttunen
    Neurobiology of Disease Laboratory, Genetics, and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease MIND and Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA
    J Mol Neurosci 37:6-15. 2009
    ....
  5. ncbi request reprint HtrA2 regulates beta-amyloid precursor protein (APP) metabolism through endoplasmic reticulum-associated degradation
    Henri J Huttunen
    Neurobiology of Disease Laboratory, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA
    J Biol Chem 282:28285-95. 2007
    ..Based on these results we suggest a novel function for HtrA2 as a regulator of APP metabolism through ER-associated degradation...
  6. pmc ACAT as a drug target for Alzheimer's disease
    Henri J Huttunen
    Neurobiology of Disease Laboratory, Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School, Charlestown, Mass 02129, USA
    Neurodegener Dis 5:212-4. 2008
    ..Here, we discuss data supporting ACAT inhibition as a strategy to treat Alzheimer's disease...
  7. ncbi request reprint The ACAT inhibitor CP-113,818 markedly reduces amyloid pathology in a mouse model of Alzheimer's disease
    Birgit Hutter-Paier
    JSW Research Forschungslabor GmbH, Institute of Experimental Pharmacology, Rankengasse 28, 8020 Graz, Austria
    Neuron 44:227-38. 2004
    ..Our results suggest that ACAT inhibition may be effective in the prevention and treatment of AD by inhibiting generation of the Abeta peptide...