M C Irizarry

Summary

Affiliation: Massachusetts General Hospital
Country: USA

Publications

  1. pmc Biomarkers of Alzheimer disease in plasma
    Michael C Irizarry
    Alzheimer Disease Research Unit, Department of Neurology, Massachusetts General Hospital, Charlestown, Massachusetts 02129, USA
    NeuroRx 1:226-34. 2004
  2. ncbi request reprint Association of homocysteine with plasma amyloid beta protein in aging and neurodegenerative disease
    M C Irizarry
    The Massachusetts Alzheimer Disease Research Center, Massachusetts General Hospital, Boston, MA, USA
    Neurology 65:1402-8. 2005
  3. ncbi request reprint Plasma beta-amyloid and white matter lesions in AD, MCI, and cerebral amyloid angiopathy
    M E Gurol
    Department of Neurology, Massachusetts General Hospital, Boston, MA 02114, USA
    Neurology 66:23-9. 2006
  4. ncbi request reprint Plaque-induced abnormalities in neurite geometry in transgenic models of Alzheimer disease: implications for neural system disruption
    R Le
    Department of Neurology, Massachusetts General Hospital, Charlestown, USA
    J Neuropathol Exp Neurol 60:753-8. 2001
  5. ncbi request reprint Modulation of A beta deposition in APP transgenic mice by an apolipoprotein E null background
    M C Irizarry
    Alzheimer Disease Research Unit, Massachusetts General Hospital East, 149 13th Street, Charlestown, MA 02129, USA
    Ann N Y Acad Sci 920:171-8. 2000
  6. pmc beta-site APP cleaving enzyme mRNA expression in APP transgenic mice: anatomical overlap with transgene expression and static levels with aging
    M C Irizarry
    Alzheimer Disease Research Unit, Massachusetts General Hospital, Charlestown, MA 02129, USA
    Am J Pathol 158:173-7. 2001
  7. ncbi request reprint Glutamate receptor dysregulation in the hippocampus of transgenic mice carrying mutated human amyloid precursor protein
    J H Cha
    Department of Neurology, Massachusetts General Hospital, Boston, Massachusetts, USA
    Neurobiol Dis 8:90-102. 2001
  8. ncbi request reprint Early Abeta accumulation and progressive synaptic loss, gliosis, and tangle formation in AD brain
    M Ingelsson
    Harvard Medical School, Massachusetts General Hospital, Boston
    Neurology 62:925-31. 2004
  9. pmc Plasma Abeta, homocysteine, and cognition: the Vitamin Intervention for Stroke Prevention (VISP) trial
    A Viswanathan
    Hemorrhagic Stroke Research Program, Massachusetts General Hospital Stroke Research Center, 175 Cambridge Street, Suite 300, Boston, MA 02114, USA
    Neurology 72:268-72. 2009
  10. pmc Neurotoxic effects of thioflavin S-positive amyloid deposits in transgenic mice and Alzheimer's disease
    B Urbanc
    Center for Polymer Studies and Department of Physics, Boston University, Boston, MA 02215, USA
    Proc Natl Acad Sci U S A 99:13990-5. 2002

Collaborators

Detail Information

Publications48

  1. pmc Biomarkers of Alzheimer disease in plasma
    Michael C Irizarry
    Alzheimer Disease Research Unit, Department of Neurology, Massachusetts General Hospital, Charlestown, Massachusetts 02129, USA
    NeuroRx 1:226-34. 2004
    ....
  2. ncbi request reprint Association of homocysteine with plasma amyloid beta protein in aging and neurodegenerative disease
    M C Irizarry
    The Massachusetts Alzheimer Disease Research Center, Massachusetts General Hospital, Boston, MA, USA
    Neurology 65:1402-8. 2005
    ..tHcy may potentiate neurotoxic and vasculopathic processes, including amyloid beta protein (Abeta) metabolism, implicated in neurodegenerative diseases...
  3. ncbi request reprint Plasma beta-amyloid and white matter lesions in AD, MCI, and cerebral amyloid angiopathy
    M E Gurol
    Department of Neurology, Massachusetts General Hospital, Boston, MA 02114, USA
    Neurology 66:23-9. 2006
    ..Recent studies suggest a role for circulating beta-amyloid peptide in microvascular dysfunction and white matter disease...
  4. ncbi request reprint Plaque-induced abnormalities in neurite geometry in transgenic models of Alzheimer disease: implications for neural system disruption
    R Le
    Department of Neurology, Massachusetts General Hospital, Charlestown, USA
    J Neuropathol Exp Neurol 60:753-8. 2001
    ....
  5. ncbi request reprint Modulation of A beta deposition in APP transgenic mice by an apolipoprotein E null background
    M C Irizarry
    Alzheimer Disease Research Unit, Massachusetts General Hospital East, 149 13th Street, Charlestown, MA 02129, USA
    Ann N Y Acad Sci 920:171-8. 2000
    ....
  6. pmc beta-site APP cleaving enzyme mRNA expression in APP transgenic mice: anatomical overlap with transgene expression and static levels with aging
    M C Irizarry
    Alzheimer Disease Research Unit, Massachusetts General Hospital, Charlestown, MA 02129, USA
    Am J Pathol 158:173-7. 2001
    ..Thus, hAPP and endogenous BACE expression in similar anatomical localizations allow for processing of hAPP and Abeta formation in hAPP transgenic mice, but these are modified by additional age-related and anatomical factors...
  7. ncbi request reprint Glutamate receptor dysregulation in the hippocampus of transgenic mice carrying mutated human amyloid precursor protein
    J H Cha
    Department of Neurology, Massachusetts General Hospital, Boston, Massachusetts, USA
    Neurobiol Dis 8:90-102. 2001
    ..These data suggest that mutant APP overexpression or age-related amyloid deposition produce a subtle specific alteration in hippocampal glutamate receptors with aging...
  8. ncbi request reprint Early Abeta accumulation and progressive synaptic loss, gliosis, and tangle formation in AD brain
    M Ingelsson
    Harvard Medical School, Massachusetts General Hospital, Boston
    Neurology 62:925-31. 2004
    ..Pathologic changes in the Alzheimer disease (AD) brain occur in a hierarchical neuroanatomical pattern affecting cortical, subcortical, and limbic regions...
  9. pmc Plasma Abeta, homocysteine, and cognition: the Vitamin Intervention for Stroke Prevention (VISP) trial
    A Viswanathan
    Hemorrhagic Stroke Research Program, Massachusetts General Hospital Stroke Research Center, 175 Cambridge Street, Suite 300, Boston, MA 02114, USA
    Neurology 72:268-72. 2009
    ....
  10. pmc Neurotoxic effects of thioflavin S-positive amyloid deposits in transgenic mice and Alzheimer's disease
    B Urbanc
    Center for Polymer Studies and Department of Physics, Boston University, Boston, MA 02215, USA
    Proc Natl Acad Sci U S A 99:13990-5. 2002
    ..These results, along with computer simulations, suggest that Abeta develops neurotoxic properties in vivo when it adopts a fibrillar beta-pleated sheet conformation...
  11. ncbi request reprint Plasma F2A isoprostane levels in Alzheimer's and Parkinson's disease
    M C Irizarry
    Massachusetts Alzheimer s Disease Research Center, Massachusetts General Hospital, Boston, MA, USA
    Neurodegener Dis 4:403-5. 2007
    ..F2-isoprostane is a marker of lipid peroxidation which is elevated in AD CSF. Plasma F2-isoprostane has been proposed as a diagnostic marker for AD and mild cognitive impairment (MCI)...
  12. ncbi request reprint Clinical and biochemical correlates of insoluble alpha-synuclein in dementia with Lewy bodies
    J Klucken
    Department of Neurology, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, 114 16th Street, Charlestown, MA 02129, USA
    Acta Neuropathol 111:101-8. 2006
    ..However, the Triton X-100 soluble fraction of alpha-synuclein did correlate strongly with the expression of several heat shock proteins (HSPs) in DLB but not control cases, suggesting a coordinated HSP response in DLB neocortex...
  13. ncbi request reprint Alzheimer disease therapeutics
    M C Irizarry
    Alzheimer Disease Research Unit, Center for Aging Genetics and Neurodegeneration, Massachusetts General Hospital, Boston, USA
    J Neuropathol Exp Neurol 60:923-8. 2001
    ..Rational neuroprotective approaches have led to recent trials of estrogen, antioxidant and anti-inflammatory medications in AD, and to the development of anti-amyloid strategies for delaying progression or preventing development of AD...
  14. ncbi request reprint Alpha-synuclein has an altered conformation and shows a tight intermolecular interaction with ubiquitin in Lewy bodies
    N Sharma
    Department of Neurology, Massachusetts General Hospital East, Charlestown 02129, USA
    Acta Neuropathol 102:329-34. 2001
    ..These observations provide support for the hypothesis that in Lewy bodies alpha-synuclein adopts an altered three-dimensional structure and undergoes N-terminal ubiquitination...
  15. pmc Elevation of cystatin C in susceptible neurons in Alzheimer's disease
    A Deng
    Memory Disorders Clinic and the Alzheimer's Research Unit, Department of Neurology, Massachusetts General Hospital, Boston, Massachusetts, USA
    Am J Pathol 159:1061-8. 2001
    ..These neuropathological observations reinforce the association between cystatin C and AD, and support a model of cystatin C involvement in the process of neuronal death in AD...
  16. ncbi request reprint Apolipoprotein E facilitates neuritic and cerebrovascular plaque formation in an Alzheimer's disease model
    D M Holtzman
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    Ann Neurol 47:739-47. 2000
    ..These data demonstrate that ApoE facilitates the formation of both neuritic and cerebrovascular plaques, which are pathological hallmarks of AD and cerebral amyloid angiopathy...
  17. ncbi request reprint Relation of quantitative indexes of concurrent alpha-synuclein abnormalities to clinical outcome in autopsy-proven Alzheimer disease
    Roee Holtzer
    Sergievsky Center, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA
    Arch Neurol 63:226-30. 2006
    ..Most studies used semiquantitative measures to determine the presence or absence of LB abnormalities...
  18. ncbi request reprint Coordinated expression of caspase 8, 3 and 7 mRNA in temporal cortex of Alzheimer disease: relationship to formic acid extractable abeta42 levels
    Toshifumi Matsui
    Alzheimer Research Unit, Mass General Institute for Neurodegenerative Disease, Massachusetts General Hospital, Charlestown, Massachusetts 02129, USA
    J Neuropathol Exp Neurol 65:508-15. 2006
    ..Thus, a principal caspase pathway from caspase-8 to caspase-3 and/or 7 may contribute to neuron loss in AD brain...
  19. ncbi request reprint Prevalence and effects of lobar microhemorrhages in early-stage dementia
    Alireza Atri
    Department of Neurology, Massachusetts General Hospital, Boston, MA, USA
    Neurodegener Dis 2:305-12. 2005
    ..The prevalence and effects of LMH detectable by gradient echo MRI (GE-MRI) in early-stage dementia are unknown...
  20. ncbi request reprint Molecular imaging with Pittsburgh Compound B confirmed at autopsy: a case report
    Brian J Bacskai
    MassGeneral Institute for Neurodegenerative Diseases, Department of Neurology, Charlestown, MA 02129, USA
    Arch Neurol 64:431-4. 2007
    ..Imaging revealed marked region specific binding of PiB and abnormal fluorodeoxyglucose uptake. Intervention Autopsy was performed 3 months after the PiB scan...
  21. ncbi request reprint The normal equilibrium between CSF and plasma amyloid beta levels is disrupted in Alzheimer's disease
    Vilmantas Giedraitis
    Department of Public Health Geriatrics, Uppsala University, Uppsala, Sweden
    Neurosci Lett 427:127-31. 2007
    ..Our findings suggest that the normal equilibrium between CSF and plasma Abeta may be disrupted with the initiation of amyloid deposition in the brain...
  22. doi request reprint Plasma beta amyloid and the risk of Alzheimer disease and dementia in elderly men: a prospective, population-based cohort study
    Johan Sundelöf
    Uppsala University, Department of Public Health and Geriatrics, Uppsala Science Park, Dag Hammarskölds väg 14B, Uppsala, Sweden
    Arch Neurol 65:256-63. 2008
    ..Beta amyloid (Abeta) protein accumulates in the brains of individuals with Alzheimer disease (AD) and is detectable in cerebrospinal fluid and plasma...
  23. pmc Plasma amyloid beta-protein and C-reactive protein in relation to the rate of progression of Alzheimer disease
    Joseph J Locascio
    Massachusetts Alzheimer s Disease Research Center, Wang Ambulatory Care Center, Suite 720, Room 731 G, Massachusetts General Hospital, 15 Parkman St, Boston, MA 02114, USA
    Arch Neurol 65:776-85. 2008
    ....
  24. ncbi request reprint Predictors of placebo group decline in the Alzheimer's disease Assessment Scale-cognitive subscale (ADAS-Cog) in 24 week clinical trials of Alzheimer's disease
    Michael C Irizarry
    WW Epidemiology, GlaxoSmithKline, Harlow, UK
    J Alzheimers Dis 14:301-11. 2008
    ..Overcoming lack of placebo decline in AD clinical trials will require scales more sensitive to cognitive decline in mild AD and strategies to reduce within-person variability in outcome measures...
  25. ncbi request reprint Decreased levels of BDNF protein in Alzheimer temporal cortex are independent of BDNF polymorphisms
    Jung Lee
    Harvard Medical School, Massachusetts General Hospital, 114 16th Street, Charlestown, MA 02129, USA
    Exp Neurol 194:91-6. 2005
    ..The results suggest that the investigated BDNF polymorphisms are neither robust genetic risk factors nor determinants of BDNF protein levels in AD...
  26. ncbi request reprint Autoantibodies to redox-modified oligomeric Abeta are attenuated in the plasma of Alzheimer's disease patients
    Robert D Moir
    Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital and Harvard Medical School, Charlestown 02129 4404, USA
    J Biol Chem 280:17458-63. 2005
    ..041) with plasma immunoreactivity to CAPS. These data suggest that autoantibodies to CAPS are depleted in AD patients and raise the prospect that immunization with anti-CAPS antibodies might provide therapeutic benefit for AD...
  27. ncbi request reprint A turn of the sulfatide in Alzheimer's disease
    Michael C Irizarry
    Ann Neurol 54:7-8. 2003
  28. ncbi request reprint Age but not diagnosis is the main predictor of plasma amyloid beta-protein levels
    Hiroaki Fukumoto
    Department of Neurology, Massachusetts General Hospital, Boston, MA 02129, USA
    Arch Neurol 60:958-64. 2003
    ..Plasma amyloid beta-protein Abeta42 levels are increased in patients with familial Alzheimer disease (AD) mutations, and high levels reportedly identify individuals at risk to develop AD...
  29. ncbi request reprint Brain isoprostanes: a marker of lipid peroxidation and oxidative stress in AD
    Michael C Irizarry
    Neurology 61:436-7. 2003
  30. ncbi request reprint APOE epsilon 3/ epsilon 4 heterozygotes have an elevated proportion of apolipoprotein E4 in cerebrospinal fluid relative to plasma, independent of Alzheimer's disease diagnosis
    Hiroaki Fukumoto
    Alzheimer Disease Research Unit, Massachusetts General Hospital East, B114 2010, 114 16th St, Charlestown, MA 02129, USA
    Exp Neurol 183:249-53. 2003
    ..However, the greater proportion of apoE4 in the cerebrospinal fluid suggests differential production or metabolism of the protein in the central nervous system (CNS), with the apoE4 isoform dominating...
  31. ncbi request reprint Lack of association of the cholesterol 24-hydroxylase (CYP46) intron 2 polymorphism with Alzheimer's disease
    Martin Ingelsson
    Harvard Medical School, Massachusetts General Hospital, 114 16th Street, Charlestown, MA 02129, USA
    Neurosci Lett 367:228-31. 2004
    ..Despite growing evidence implicating cholesterol metabolism in AD risk and Abeta generation, our data does not support a robust genetic relationship between the CYP46 intron 2 polymorphism and AD risk or neuropathology...
  32. pmc Beta-secretase activity increases with aging in human, monkey, and mouse brain
    Hiroaki Fukumoto
    Department of Neurology, Alzheimer Disease Research Unit, Massachusetts General Hospital East, Charlestown, Massachusetts 02129, USA
    Am J Pathol 164:719-25. 2004
    ..These data suggest that an age-related increase of BACE activity contributes to the increased production and accumulation of brain A beta, and potentially predisposes to Alzheimer's disease in humans...
  33. ncbi request reprint LRP and senile plaques in Alzheimer's disease: colocalization with apolipoprotein E and with activated astrocytes
    Katrin Arelin
    Alzheimer Research Unit, Department of Neurology, Massachusetts General Hospital, 114 16th Street, Room 2009, Charlestown, MA 02129, USA
    Brain Res Mol Brain Res 104:38-46. 2002
    ..The upregulation of LRP would allow increased clearance of LRP ligands as well as clearance of Abeta/ApoE complexes...
  34. ncbi request reprint Beta-secretase protein and activity are increased in the neocortex in Alzheimer disease
    Hiroaki Fukumoto
    Alzheimer Disease Research Unit, Center for Aging, Genetics, and Neurodegeneration, Massachusetts General Hospital East, Bldg 114, Room 2010, 114 16th Street, Charlestown, MA 02129, USA
    Arch Neurol 59:1381-9. 2002
    ....
  35. doi request reprint Genotyping of apolipoprotein E: comparative evaluation of different protocols
    Martin Ingelsson
    Harvard Medical School Massachusetts General Hospital, Charlestown, Massachusetts, USA
    Curr Protoc Hum Genet . 2003
    ..The latter approaches also provide the flexibility to investigate other polymorphic disease markers...
  36. ncbi request reprint Induction of the cholesterol transporter ABCA1 in central nervous system cells by liver X receptor agonists increases secreted Abeta levels
    Hiroaki Fukumoto
    Alzheimer Research Unit, Massachusetts General Hospital, Charlestown 02129, USA
    J Biol Chem 277:48508-13. 2002
    ..The increase in secreted Abeta levels was reduced by RNAi blocking of ABCA1 expression. These data suggest that the cholesterol efflux molecule ABCA1 may also be involved in the secretion of the membrane-associated molecule, Abeta...
  37. ncbi request reprint Candidate single-nucleotide polymorphisms from a genomewide association study of Alzheimer disease
    Hao Li
    GlaxoSmithKline, Research Triangle Park, North Carolina, USA
    Arch Neurol 65:45-53. 2008
    ..To identify single-nucleotide polymorphisms (SNPs) associated with risk and age at onset of Alzheimer disease (AD) in a genomewide association study of 469 438 SNPs...
  38. ncbi request reprint Motor dysfunction and gliosis with preserved dopaminergic markers in human alpha-synuclein A30P transgenic mice
    Teresa Gomez-Isla
    Department of Neurology, University of Minnesota, Minneapolis, MN 55455, USA
    Neurobiol Aging 24:245-58. 2003
    ..Thus, high expression of mutant human alpha-synuclein resulted in a progressive motor and widespread CNS gliotic phenotype independent of dopaminergic dysfunction in the Tg5093 line...
  39. ncbi request reprint Demonstration by FRET of BACE interaction with the amyloid precursor protein at the cell surface and in early endosomes
    Ayae Kinoshita
    Alzheimer Disease Research Laboratory, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA
    J Cell Sci 116:3339-46. 2003
    ..Taken together, these data confirm a close APP-BACE interaction in early endosomes, and highlight the cell surface as an additional potential site of APP-BACE interaction...
  40. ncbi request reprint Increase in the relative expression of tau with four microtubule binding repeat regions in frontotemporal lobar degeneration and progressive supranuclear palsy brains
    Martin Ingelsson
    Harvard Medical School, Massachusetts General Hospital, 114 16th Street, Charlestown, MA 02129, USA
    Acta Neuropathol 114:471-9. 2007
    ..In conclusion, we demonstrated increased but largely variable 4R tau/3R tau mRNA ratios in FTLD and PSP cases, suggesting heterogeneous pathophysiological processes within these disorders...
  41. ncbi request reprint Expression of APP pathway mRNAs and proteins in Alzheimer's disease
    Toshifumi Matsui
    Alzheimer Disease Research Unit, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Charlestown, MA 02129, USA
    Brain Res 1161:116-23. 2007
    ..These results suggest that altered transcription of APP in AD is proportionately associated with Abeta peptide, may occur in the context of gliosis, and may contribute to Abeta deposition in sporadic AD...
  42. ncbi request reprint Plasma Abeta levels do not reflect brain Abeta levels
    Stefanie H Freeman
    C S Kubik Laboratory for Neuropathology, Department of Pathology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02129, USA
    J Neuropathol Exp Neurol 66:264-71. 2007
    ..We conclude that plasma levels of Abeta40 and Abeta42 are not robust correlates of histologic or biochemically assessed amyloid burdens in brain, although the influence of the APOE genotype should be further explored...
  43. ncbi request reprint Demonstration of BACE (beta-secretase) phosphorylation and its interaction with GGA1 in cells by fluorescence-lifetime imaging microscopy
    Christine A F von Arnim
    Alzheimer Disease Research Laboratory, Massachusetts General Hospital, Harvard Medical School, 114 16th Street, Charlestown, MA 02129, USA
    J Cell Sci 117:5437-45. 2004
    ....
  44. ncbi request reprint GGA1 acts as a spatial switch altering amyloid precursor protein trafficking and processing
    Christine A F von Arnim
    Alzheimer Disease Research Laboratory, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA
    J Neurosci 26:9913-22. 2006
    ..GGA1 may act as a specific spatial switch influencing APP trafficking and processing, so that APP-GGA1 interactions may have pathophysiological relevance in AD...
  45. ncbi request reprint Interaction of the cytosolic domains of sorLA/LR11 with the amyloid precursor protein (APP) and beta-secretase beta-site APP-cleaving enzyme
    Robert Spoelgen
    Alzheimer s Disease Research Laboratory, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA
    J Neurosci 26:418-28. 2006
    ..We discovered that sorLA significantly reduced BACE-APP interactions in Golgi. We postulate that sorLA acts as a trafficking receptor that prevents BACE-APP interactions and hence BACE cleavage of APP...
  46. ncbi request reprint No alteration in tau exon 10 alternative splicing in tangle-bearing neurons of the Alzheimer's disease brain
    Martin Ingelsson
    Harvard Medical School, Massachusetts General Hospital, 114 16th Street, Charlestown, MA 02129, USA
    Acta Neuropathol 112:439-49. 2006
    ..In conclusion, this study indicated region-specific and possibly cell-type-specific tau splicing but did not lend any support to overt changes in alternative splicing of tau exon 10 being an underlying factor in AD pathogenesis...
  47. ncbi request reprint Apolipoprotein E modulates gamma-secretase cleavage of the amyloid precursor protein
    Michael C Irizarry
    Alzheimer Disease Research Unit, Massachusetts General Hospital East, Charlestown, Massachusetts, USA
    J Neurochem 90:1132-43. 2004
    ..The apoE modulation of Abeta production and APP signaling is a potential mechanism affecting Alzheimer disease risk...
  48. ncbi request reprint Prospective study of plasma folate, vitamin B12, and cognitive function and decline
    Jae Hee Kang
    Department of Medicine, Channing Laboratory, Brigham and Women s Hospital, Boston, MA, USA
    Epidemiology 17:650-7. 2006
    ..The relation between B vitamins and cognitive decline is controversial. In this study, we explored the association of plasma folate and vitamin B12 with cognitive function measured approximately 10 years later...