B T Hyman

Summary

Affiliation: Harvard University
Country: USA

Publications

  1. ncbi request reprint Autoantibodies to amyloid-beta and Alzheimer's disease
    B T Hyman
    Department of Neurology, Taub Institute for Research in Alzheimer s Disease and the Aging Brain, Gertrude H Sergievsky Center, Columbia University College of Physicians and Surgeons, New York, NY, USA
    Ann Neurol 49:808-10. 2001
  2. ncbi request reprint Role of the low-density lipoprotein receptor-related protein in beta-amyloid metabolism and Alzheimer disease
    B T Hyman
    Alzheimer Disease Research Laboratory, Massachusetts General Hospital, Boston, USA
    Arch Neurol 57:646-50. 2000
  3. ncbi request reprint Direct visualization of the gamma secretase-generated carboxyl-terminal domain of the amyloid precursor protein: association with Fe65 and translocation to the nucleus
    A Kinoshita
    Alzheimer Disease Research Laboratory, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts, USA
    J Neurochem 82:839-47. 2002
  4. ncbi request reprint Effect of PS1 deficiency and an APP gamma-secretase inhibitor on Notch1 signaling in primary mammalian neurons
    C Jack
    Alzheimer s Disease Research Laboratory, Department of Neurology, Harvard Medical School, Massachusetts General Hospital, 149 13th Street, Charlestown, MA 02129, USA
    Brain Res Mol Brain Res 87:166-74. 2001
  5. ncbi request reprint Notch1 and amyloid precursor protein are competitive substrates for presenilin1-dependent gamma-secretase cleavage
    O Berezovska
    Alzheimer's Disease Research Laboratory, Department of Neurology, Harvard Medical School, Massachusetts General Hospital, Charlestown, Massachusetts 02129, USA
    J Biol Chem 276:30018-23. 2001
  6. 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
  7. ncbi request reprint Rapid Notch1 nuclear translocation after ligand binding depends on presenilin-associated gamma-secretase activity
    O Berezovska
    Alzheimer s Disease Research Laboratory, Massachusetts General Hospital, 149 13th Street, Charlestown, MA 02129, USA
    Ann N Y Acad Sci 920:223-6. 2000
  8. pmc Temporoparietal MR imaging measures of atrophy in subjects with mild cognitive impairment that predict subsequent diagnosis of Alzheimer disease
    R S Desikan
    Department of Anatomy and Neurobiology, Boston University School of Medicine, Boston, MA 02118, USA
    AJNR Am J Neuroradiol 30:532-8. 2009
  9. ncbi request reprint Alpha-synuclein-enhanced green fluorescent protein fusion proteins form proteasome sensitive inclusions in primary neurons
    P J McLean
    Alzheimer's Disease Research Unit, Department of Neurology, Rm 6405, Massachusetts General Hospital East, 149, 13th Street, Charlestown, MA 02129, USA
    Neuroscience 104:901-12. 2001
  10. 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

Detail Information

Publications70

  1. ncbi request reprint Autoantibodies to amyloid-beta and Alzheimer's disease
    B T Hyman
    Department of Neurology, Taub Institute for Research in Alzheimer s Disease and the Aging Brain, Gertrude H Sergievsky Center, Columbia University College of Physicians and Surgeons, New York, NY, USA
    Ann Neurol 49:808-10. 2001
    ..These data suggest that low levels of anti-amyloid-beta autoantibodies are frequent in the elderly population but do not confer protection against developing dementia...
  2. ncbi request reprint Role of the low-density lipoprotein receptor-related protein in beta-amyloid metabolism and Alzheimer disease
    B T Hyman
    Alzheimer Disease Research Laboratory, Massachusetts General Hospital, Boston, USA
    Arch Neurol 57:646-50. 2000
    ..The LRP also interacts with the amyloid precursor protein itself. In this review, we highlight data that support a role for LRP in A beta metabolism and hypothesize that LRP therefore plays a critical role in Alzheimer disease...
  3. ncbi request reprint Direct visualization of the gamma secretase-generated carboxyl-terminal domain of the amyloid precursor protein: association with Fe65 and translocation to the nucleus
    A Kinoshita
    Alzheimer Disease Research Laboratory, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts, USA
    J Neurochem 82:839-47. 2002
    ..Visualization of the APP-CT-Fe65 complex in the nucleus may serve as a readout for processes that modify gamma secretase release of APP-CT...
  4. ncbi request reprint Effect of PS1 deficiency and an APP gamma-secretase inhibitor on Notch1 signaling in primary mammalian neurons
    C Jack
    Alzheimer s Disease Research Laboratory, Department of Neurology, Harvard Medical School, Massachusetts General Hospital, 149 13th Street, Charlestown, MA 02129, USA
    Brain Res Mol Brain Res 87:166-74. 2001
    ..These results support the hypothesis that PS1 deficiency blocks neuronal Notch1 processing and signaling...
  5. ncbi request reprint Notch1 and amyloid precursor protein are competitive substrates for presenilin1-dependent gamma-secretase cleavage
    O Berezovska
    Alzheimer's Disease Research Laboratory, Department of Neurology, Harvard Medical School, Massachusetts General Hospital, Charlestown, Massachusetts 02129, USA
    J Biol Chem 276:30018-23. 2001
    ..In summary, two complementary approaches suggest that APP and Notch1 are physiologically relevant competitive substrates for gamma-secretase activity...
  6. 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
    ....
  7. ncbi request reprint Rapid Notch1 nuclear translocation after ligand binding depends on presenilin-associated gamma-secretase activity
    O Berezovska
    Alzheimer s Disease Research Laboratory, Massachusetts General Hospital, 149 13th Street, Charlestown, MA 02129, USA
    Ann N Y Acad Sci 920:223-6. 2000
    ....
  8. pmc Temporoparietal MR imaging measures of atrophy in subjects with mild cognitive impairment that predict subsequent diagnosis of Alzheimer disease
    R S Desikan
    Department of Anatomy and Neurobiology, Boston University School of Medicine, Boston, MA 02118, USA
    AJNR Am J Neuroradiol 30:532-8. 2009
    ..Mild cognitive impairment (MCI) represents a transitional state between normal aging and Alzheimer disease (AD). Our goal was to determine if specific temporoparietal regions can predict the time to progress from MCI to AD...
  9. ncbi request reprint Alpha-synuclein-enhanced green fluorescent protein fusion proteins form proteasome sensitive inclusions in primary neurons
    P J McLean
    Alzheimer's Disease Research Unit, Department of Neurology, Rm 6405, Massachusetts General Hospital East, 149, 13th Street, Charlestown, MA 02129, USA
    Neuroscience 104:901-12. 2001
    ..Our finding that manipulations of the carboxy-terminus of alpha-synuclein lead to inclusion formation may provide a model for studies of the pathogenic mechanisms of alpha-synuclein aggregation in Lewy bodies...
  10. 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...
  11. ncbi request reprint Growth arrest of individual senile plaques in a model of Alzheimer's disease observed by in vivo multiphoton microscopy
    R H Christie
    Alzheimer's Disease Research Unit, Massachusetts General Hospital, Charlestown, Massachusetts 02129, USA
    J Neurosci 21:858-64. 2001
    ..These results indicate that thioflavine S-positive plaques appear and then are stable, supporting a dynamic feedback model of plaque growth...
  12. ncbi request reprint In vivo multiphoton imaging of a transgenic mouse model of Alzheimer disease reveals marked thioflavine-S-associated alterations in neurite trajectories
    J D D'Amore
    Neurology Service, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA
    J Neuropathol Exp Neurol 62:137-45. 2003
    ..These results support the hypothesis that compact thioflavine-S-positive plaques disrupt the neuropil in AD...
  13. ncbi request reprint Association of membrane-bound amyloid precursor protein APP with the apolipoprotein E receptor LRP
    G W Rebeck
    Alzheimer Research Unit, 149 13th Street, Massachusetts General Hospital, Charlestown, MA 02129, USA
    Brain Res Mol Brain Res 87:238-45. 2001
    ..We propose that full-length APP can transiently interact with the receptor LRP on the cell surface, affecting the processing and intracellular transport of APP...
  14. ncbi request reprint Acyl-coenzyme A: cholesterol acyltransferase modulates the generation of the amyloid beta-peptide
    L Puglielli
    Genetics and Aging Research Unit, Massachusetts General Hospital, Harvard Medical School, Building 114, 16th Street, Charlestown, Massachusetts 02129-4404, USA
    Nat Cell Biol 3:905-12. 2001
    ..We also show that pharmacological inhibitors of ACAT, developed for the treatment of atherosclerosis, are potent modulators of Abeta generation, indicating their potential for use in the treatment of Alzheimer's disease...
  15. pmc Alzheimer-signature MRI biomarker predicts AD dementia in cognitively normal adults
    B C Dickerson
    Department of Neurology, Massachusetts Alzheimer s Disease Research Center, Massachusetts General Hospital, MA, USA
    Neurology 76:1395-402. 2011
    ....
  16. ncbi request reprint Demonstration by fluorescence resonance energy transfer of two sites of interaction between the low-density lipoprotein receptor-related protein and the amyloid precursor protein: role of the intracellular adapter protein Fe65
    A Kinoshita
    Alzheimer s Disease Research Unit, Department of Neurology, Massachusetts General Hospital, Charlestown, Massachusetts 02129, USA
    J Neurosci 21:8354-61. 2001
    ..These findings demonstrate that LRP interaction with APP occurs via both extracellular and intracellular protein interaction domains...
  17. ncbi request reprint The impact of different presenilin 1 andpresenilin 2 mutations on amyloid deposition, neurofibrillary changes and neuronal loss in the familial Alzheimer's disease brain: evidence for other phenotype-modifying factors
    T Gomez-Isla
    Neurology Service, Massachusetts General Hospital, Neurology Service, Brigham and Women s Hospital, Boston, USA
    Brain 122:1709-19. 1999
    ..This suggests that further individual or pedigree genetic or epigenetic factors are likely to modulate PS phenotypes strongly...
  18. ncbi request reprint Lack of independent associations of apolipoprotein E promoter and intron 1 polymorphisms with Alzheimer's disease
    G W Rebeck
    Alzheimer Research Unit, Massachusetts General Hospital, Charlestown 02129, USA
    Neurosci Lett 272:155-8. 1999
    ..Controlling for these linkages, we found no independent association between the -219 polymorphism and AD or CAA. Thus, our studies do not support independent associations between AD and either the IE-1 or the -219 polymorphisms...
  19. ncbi request reprint Analysis of cerebral amyloid angiopathy in a transgenic mouse model of Alzheimer disease using in vivo multiphoton microscopy
    E Y Kimchi
    Department of Neurology, Massachusetts General Hospital, Charlestown 02129, USA
    J Neuropathol Exp Neurol 60:274-9. 2001
    ..Taken together, these data suggest that CAA has a substantial effect on the physiology of the microvasculature in vivo...
  20. 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...
  21. ncbi request reprint Curcumin labels amyloid pathology in vivo, disrupts existing plaques, and partially restores distorted neurites in an Alzheimer mouse model
    M Garcia-Alloza
    Department of Neurology Alzheimer s Disease Research Laboratory, Massachusetts General Hospital, Charlestown, Massachusetts 02129, USA
    J Neurochem 102:1095-104. 2007
    ..This approach could lead to more effective clinical therapies for the prevention of oxidative stress, inflammation and neurotoxicity associated with AD...
  22. pmc A close association of torsinA and alpha-synuclein in Lewy bodies: a fluorescence resonance energy transfer study
    N Sharma
    Department of Neurology, Alzheimer s Disease Research Unit, and the Department of Neurology, Molecular Neurogenetics Unit, Massachusetts General Hospital East, Charlestown, Massachusetts Albert Einstein College of Medicine, Bronx, New York
    Am J Pathol 159:339-44. 2001
    ..Using sensitive fluorescent resonance energy transfer (FRET) techniques, we find evidence of a close association between torsinA and alpha-synuclein in Lewy bodies...
  23. 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...
  24. ncbi request reprint An investigation of clinical correlates of Lewy bodies in autopsy-proven Alzheimer disease
    Y Stern
    Department of Neurology and Gertrude H Sergievsky Center, Columbia University College of Physicians and Surgeons, 630 W 168th St, New York, NY 10032, USA
    Arch Neurol 58:460-5. 2001
    ....
  25. 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...
  26. ncbi request reprint Elevation of LDL receptor-related protein levels via ligand interactions in Alzheimer disease and in vitro
    Z Qiu
    Alzheimer Research Unit, Massachusetts General Hospital, Harvard Medical School, Boston, USA
    J Neuropathol Exp Neurol 60:430-40. 2001
    ....
  27. 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
    ....
  28. 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...
  29. ncbi request reprint Uptake of fibrillar beta-amyloid by microglia isolated from MSR-A (type I and type II) knockout mice
    H Chung
    Department of Biochemistry, Weill Medical College of Cornell University, Room E215, 1300 York Avenue, New York, NY 10021, USA
    Neuroreport 12:1151-4. 2001
    ..Uptake of modified fA beta (ClqA beta) was similar in the MSR-A-/- microglia as in the wildtype indicating that the uptake of the opsonized fA beta is independent of MSR-A...
  30. ncbi request reprint No evidence for genetic association or linkage of the cathepsin D (CTSD) exon 2 polymorphism and Alzheimer disease
    L Bertram
    Genetics and Aging Unit, Massachusetts General Hospital, Harvard Medical School, Charlestown, USA
    Ann Neurol 49:114-6. 2001
    ..Thus, our analyses on more than 800 subjects suggest that if an association between the CTSD exon 2 polymorphism and AD exists, it is likely to be smaller than previously reported...
  31. ncbi request reprint Aspartate mutations in presenilin and gamma-secretase inhibitors both impair notch1 proteolysis and nuclear translocation with relative preservation of notch1 signaling
    O Berezovska
    Alzheimer s Disease Research Laboratory, Department of Neurology, Harvard Medical School and Massachusetts General Hospital, Charlestown, California, USA
    J Neurochem 75:583-93. 2000
    ..The latter is an important finding from the perspective of therapeutic treatment of Alzheimer's disease by targeting gamma-secretase processing of APP to reduce Abeta production...
  32. 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...
  33. pmc Immunohistochemical study of the beta-chemokine receptors CCR3 and CCR5 and their ligands in normal and Alzheimer's disease brains
    M Q Xia
    Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown 02129, USA
    Am J Pathol 153:31-7. 1998
    ....
  34. ncbi request reprint Evidence against association of the FE65 gene (APBB1) intron 13 polymorphism in Alzheimer's patients
    S Y Guenette
    Genetics and Aging Unit, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA
    Neurosci Lett 296:17-20. 2000
    ..We conclude that the association of the FE65 intron 13 polymorphism with AD, if any, is smaller than previously reported...
  35. ncbi request reprint ApoE isoforms affect neuronal N-methyl-D-aspartate calcium responses and toxicity via receptor-mediated processes
    Z Qiu
    Department of Neurology, Massachusetts General Hospital, 114 16th Street, Charlestown, MA 02129, USA
    Neuroscience 122:291-303. 2003
    ..Taken together, our data demonstrate that differential effects of apoE3 and apoE4 on the calcium signaling in neurons correlate with their effect on neurotoxicity, which are secondary to receptor binding...
  36. pmc Neuron recognition by parallel Potts segmentation
    S Peng
    Center for Polymer Studies and Department of Physics, Boston University, Boston, MA 02215, USA
    Proc Natl Acad Sci U S A 100:3847-52. 2003
    ..We apply our parallel segmentation method to control individuals and to AD patients and achieve recognition of 98% (for a control) and 93% (for an AD patient), with at most 3% false clusters...
  37. 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)...
  38. pmc Interaction of the apolipoprotein E receptors low density lipoprotein receptor-related protein and sorLA/LR11
    R Spoelgen
    Department of Neurology, Massachusetts General Hospital, Harvard Medical School, MA 02129, USA
    Neuroscience 158:1460-8. 2009
    ....
  39. ncbi request reprint Multiphoton microscopy and amyloid angiopathy
    R Christie
    Alzheimer's Disease Research Unit, Massachusetts General Hospital, Boston, 02114, USA
    Amyloid 8:48-50. 2001
    ..We also present a novelform of microscopy that allows in vivo imaging of vessels affected by amyloid in the anesthetized, but intact, animal...
  40. 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...
  41. ncbi request reprint Effects of aging on quinolinic acid lesions in rat striatum
    S F Finn
    Neurochemistry Laboratory, Massachusetts General Hospital, Boston
    Brain Res 562:276-80. 1991
    ..The delayed onset of several neurodegenerative illnesses is therefore unlikely to be due to an increasing susceptibility to excitotoxin lesions with aging...
  42. ncbi request reprint Quantitation of apoE domains in Alzheimer disease brain suggests a role for apoE in Abeta aggregation
    H S Cho
    Alzheimer Research Unit, Massachusetts General Hospital, Boston 02129, USA
    J Neuropathol Exp Neurol 60:342-9. 2001
    ..Furthermore, the presence of the apoE receptor binding domain in the center of amyloid deposits could affect surrounding cells via chronic interactions with cell surface apoE receptors...
  43. ncbi request reprint Cortical neurons expressing calcium binding proteins are spared in dementia with Lewy bodies
    E Gomez-Tortosa
    Neurology Department, Massachusetts General Hospital, Charlestown 02129, USA
    Acta Neuropathol 101:36-42. 2001
    ..However, the majority of cortical LB develop in neurons not identified by any of these markers...
  44. ncbi request reprint Amyloid beta-peptide is transported on lipoproteins and albumin in human plasma
    A L Biere
    Department of Neurology, Massachusetts General Hospital, Boston, Massachusetts 02115, USA
    J Biol Chem 271:32916-22. 1996
    ..Abeta distribution in plasma was not significantly influenced by apolipoprotein E genotype. We conclude that Abeta is normally bound to and transported by albumin and specific lipoproteins in human plasma under physiological conditions...
  45. ncbi request reprint Biochemical and immunocytochemical characterization of calsenilin in mouse brain
    N F Zaidi
    Genetics and Aging Unit, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, 114, 16th Street, Charlestown, MA 02129, USA
    Neuroscience 114:247-63. 2002
    ..Finally, the expression pattern of calsenilin, which is similar to that of the presenilin(s), suggests that the common locations of these two proteins provide an opportunity for physical interaction in vivo...
  46. 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...
  47. ncbi request reprint Expression of the chemokine receptor CXCR3 on neurons and the elevated expression of its ligand IP-10 in reactive astrocytes: in vitro ERK1/2 activation and role in Alzheimer's disease
    M Q Xia
    Alzheimer s Research, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Harvard, MA 02129, USA
    J Neuroimmunol 108:227-35. 2000
    ..Moreover, we showed that CXCR3 ligands, IP-10 and Mig, were able to activate ERK1/2 pathway in mouse cortical neurons, suggesting a novel mechanism of neuronal-glial interaction...
  48. pmc Imaging amyloid deposition in Lewy body diseases
    S N Gomperts
    Massachusetts General Hospital, Boston, MA 02114, USA
    Neurology 71:903-10. 2008
    ..In addition to widespread distribution of Lewy bodies, both diseases have variable burdens of neuritic plaques and neurofibrillary tangles characteristic of Alzheimer disease (AD)...
  49. 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
    ....
  50. pmc Activation of glycogen synthase kinase-3 beta mediates β-amyloid induced neuritic damage in Alzheimer's disease
    B Darocha-Souto
    Neurology Department, Massachusetts General Hospital, Harvard University, Boston, MA, USA
    Neurobiol Dis 45:425-37. 2012
    ....
  51. pmc MRI measures of temporoparietal regions show differential rates of atrophy during prodromal AD
    R S Desikan
    Dept of Anatomy and Neurobiology, Boston University School of Medicine, Boston, MA 02118, USA
    Neurology 71:819-25. 2008
    ..The current study was designed to determine whether a broader set of temporoparietal regions show differential rates of atrophy during the evolution of AD...
  52. ncbi request reprint Molecular and anatomical studies in Alzheimer's disease
    B T Hyman
    Alzheimer Research Unit, Massachusetts General Hospital, Charlestown, MA, USA
    Neurologia 16:100-4. 2001
    ..With this new technique, we can, for the first time, study dynamic processes of A beta deposition and resolution in a living brain...
  53. ncbi request reprint Expression and alternate splicing of apolipoprotein E receptor 2 in brain
    A E Clatworthy
    Alzheimer Research Unit, Massachusetts General Hospital, Boston 02129, USA
    Neuroscience 90:903-11. 1999
    ..Thus, apolipoprotein E receptor 2 is the fourth apolipoprotein E receptor identified on neuronal cells...
  54. ncbi request reprint Interaction of alpha-synuclein and synphilin-1: effect of Parkinson's disease-associated mutations
    H Kawamata
    Alzheimer s Disease Research Unit, Department of Neurology, Massachusetts General Hospital East, Charlestown 02129, USA
    J Neurochem 77:929-34. 2001
    ....
  55. ncbi request reprint Notch is expressed in adult brain, is coexpressed with presenilin-1, and is altered in Alzheimer disease
    O Berezovska
    Alzheimer Research Unit, Massachusetts General Hospital, Charlestown 02129, USA
    J Neuropathol Exp Neurol 57:738-45. 1998
    ..The alteration in Notch1 expression in sporadic Alzheimer disease raises the possibility that disruption of Notch1/PS-1 functional interactions may occur in Alzheimer disease...
  56. ncbi request reprint Immunohistochemical and in situ analysis of amyloid precursor-like protein-1 and amyloid precursor-like protein-2 expression in Alzheimer disease and aged control brains
    M J McNamara
    Alzheimer Research Unit, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA
    Brain Res 804:45-51. 1998
    ..The regional, cellular, and subcellular distribution of APLP1 and APLP2 overlap with each other and with APP. These observations support the hypothesis that the members of this family of proteins may perform similar functions...
  57. ncbi request reprint Developmental regulation of presenilin mRNA expression parallels notch expression
    O Berezovska
    Alzheimer Research Unit, Laboratory of Genetics and Aging, Massachusetts General Hospital, Harvard Medical School, Boston 02114, USA
    J Neuropathol Exp Neurol 56:40-4. 1997
    ..These observations show that, like Notch, PS1 and PS2 are strongly developmentally regulated, and support the plausibility of an interaction between PSs and Notch...
  58. pmc BNaC1 and BNaC2 constitute a new family of human neuronal sodium channels related to degenerins and epithelial sodium channels
    J Garcia-Anoveros
    Department of Neurobiology, Massachusetts General Hospital, Harvard Medical School, Boston 02114, USA
    Proc Natl Acad Sci U S A 94:1459-64. 1997
    ..By analogy to the ENaCs and the degenerins, which form heteromultimeric channels, BNaC1 and BNaC2 may be subunits of the same channel...
  59. ncbi request reprint Mechanisms of reduced striatal NMDA excitotoxicity in type I nitric oxide synthase knock-out mice
    C Ayata
    Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts, 02129, USA
    J Neurosci 17:6908-17. 1997
    ..The mechanism of protection in nNOS-/- mice may relate to decreased oxygen free radical production and related NO reaction products and, in part, involves mechanisms of neuronal death associated with the delayed appearance of apoptosis...
  60. ncbi request reprint MPP+ induced substantia nigra degeneration is attenuated in nNOS knockout mice
    R T Matthews
    Neurochemistry Laboratory, Massachusetts General Hospital, Boston, USA
    Neurobiol Dis 4:114-21. 1997
    ..These results provide further evidence that neuronally derived NO and peroxynitrite play a role in MPP+ neurotoxicity...
  61. ncbi request reprint Glycogen synthase kinase 3 alpha and 3 beta do not colocalize with neurofibrillary tangles
    S D Harr
    Neurology Service, Massachusetts General Hospital, Boston, USA
    Neurobiol Aging 17:343-8. 1996
    ..Interpreted within the limitations of immunohistochemical detection, these results argue against a major role of GSK 3 alpha or GSK 3 beta in NFT formation in AD...
  62. ncbi request reprint Alpha-2 macroglobulin is genetically associated with Alzheimer disease
    D Blacker
    Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, USA
    Nat Genet 19:357-60. 1998
    ....
  63. ncbi request reprint Genetic association of a cystatin C gene polymorphism with late-onset Alzheimer disease
    U Finckh
    Division of Psychiatry Research, University of Zurich, August Forel Str 1, 8008 Zurich, Switzerland
    Arch Neurol 57:1579-83. 2000
    ..To determine whether the cystatin C gene (CST3) is genetically associated with late-onset Alzheimer disease (AD)...
  64. pmc Neuropathology and apolipoprotein E profile of aged chimpanzees: implications for Alzheimer disease
    M Gearing
    Department of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA 30322
    Proc Natl Acad Sci U S A 91:9382-6. 1994
    ....
  65. ncbi request reprint Isolation and characterization of APLP2 encoding a homologue of the Alzheimer's associated amyloid beta protein precursor
    W Wasco
    Laboratory of Genetics and Aging, Massachusetts General Hospital, Charlestown 02129
    Nat Genet 5:95-100. 1993
    ..Like APP, APLP2 contains a cytoplasmic domain predicted to couple with the GTP-binding protein G(o) indicating that it may be an additional cell surface activator of this G protein...
  66. ncbi request reprint Alzheimer-associated presenilins 1 and 2: neuronal expression in brain and localization to intracellular membranes in mammalian cells
    D M Kovacs
    Genetics and Aging Unit, Massachusetts General Hospital East, Harvard Medical School, Charlestown 02129, USA
    Nat Med 2:224-9. 1996
    ....
  67. pmc Serum cystatin C and the risk of Alzheimer disease in elderly men
    J Sundelof
    Uppsala University, Department of Public Health Geriatrics, Uppsala Science Park, Uppsala, Sweden
    Neurology 71:1072-9. 2008
    ..Multiple lines of research suggest that increased cystatin C activity in the brain protects against the development of Alzheimer disease (AD)...
  68. pmc Age-related amyloid beta deposition in transgenic mice overexpressing both Alzheimer mutant presenilin 1 and amyloid beta precursor protein Swedish mutant is not associated with global neuronal loss
    A Takeuchi
    Department of Neuropathology and Neuroscience, Graduate School of Pharmaceutical Sciences, University of Tokyo, Japan
    Am J Pathol 157:331-9. 2000
    ....
  69. ncbi request reprint MRI measures of entorhinal cortex vs hippocampus in preclinical AD
    R J Killiany
    Department of Anatomy and Neurobiology, Boston University, MA, USA
    Neurology 58:1188-96. 2002
    ..MRI measures of the entorhinal cortex and the hippocampus have been used to predict which nondemented individuals with memory problems will progress to meet criteria for AD on follow-up, but their relative accuracy remains controversial...
  70. ncbi request reprint Alzheimer disease's double-edged vaccine
    S M Greenberg
    Nat Med 9:389-90. 2003