Brian Bacskai

Summary

Affiliation: Massachusetts General Hospital
Country: USA

Publications

  1. pmc Ultrasound enhanced delivery of molecular imaging and therapeutic agents in Alzheimer's disease mouse models
    Scott B Raymond
    The Harvard MIT Division of Health Sciences and Technology, Cambridge, Massachusetts, United States of America
    PLoS ONE 3:e2175. 2008
  2. ncbi request reprint Fluorescence resonance energy transfer determinations using multiphoton fluorescence lifetime imaging microscopy to characterize amyloid-beta plaques
    Brian J Bacskai
    Massachusetts General Hospital, Department of Neurology Alzheimer s Disease Research Laboratory, 114 16th Street, Charlestown, Massachusetts 02129, USA
    J Biomed Opt 8:368-75. 2003
  3. pmc Cerebrovascular lesions induce transient β-amyloid deposition
    Monica Garcia-Alloza
    Alzheimer Research Unit, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, 114 16th Street, Charlestown, MA 02129, USA
    Brain 134:3697-707. 2011
  4. 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
  5. pmc Four-dimensional multiphoton imaging of brain entry, amyloid binding, and clearance of an amyloid-beta ligand in transgenic mice
    Brian J Bacskai
    Department of Neurology Alzheimer s Disease Research Laboratory, Massachusetts General Hospital, 114 16th Street, Charlestown, MA 02129, USA
    Proc Natl Acad Sci U S A 100:12462-7. 2003
  6. pmc Existing plaques and neuritic abnormalities in APP:PS1 mice are not affected by administration of the gamma-secretase inhibitor LY-411575
    Monica Garcia-Alloza
    MassGeneral Institute for Neurodegenerative Diseases, Massachusetts General Hospital, 114 16th Street, Charlestown, MA 02129, USA
    Mol Neurodegener 4:19. 2009
  7. ncbi request reprint Reversible memory loss in a mouse transgenic model of Alzheimer's disease
    Linda A Kotilinek
    Department of Neurology, University of Minnesota, Minneapolis 55455, USA
    J Neurosci 22:6331-5. 2002
  8. pmc Differential effect of three-repeat and four-repeat tau on mitochondrial axonal transport
    Will Stoothoff
    MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA
    J Neurochem 111:417-27. 2009
  9. ncbi request reprint Preclinical characterization of amyloid imaging probes with multiphoton microscopy
    Jesse Skoch
    MassGeneral Institute for Neurodegenerative Disease, Department of Neurology Alzheimer s Disease Research Laboratory, Massachusetts General Hospital, 114 16th Street, Charlestown, MA 02129, USA
    J Alzheimers Dis 9:401-7. 2006
  10. ncbi request reprint Multiphoton imaging of ultrasound/Optison mediated cerebrovascular effects in vivo
    Scott B Raymond
    Harvard Biophysics Program, Harvard University, Boston, Massachusetts, USA
    J Cereb Blood Flow Metab 27:393-403. 2007

Research Grants

  1. Non-invasive optical imaging of neuropathology in vivo
    Brian Bacskai; Fiscal Year: 2007
  2. Mechanisms of amyloid-beta clearance.
    Brian Bacskai; Fiscal Year: 2003
  3. Mechanisms of amyloid-beta clearance.
    Brian Bacskai; Fiscal Year: 2006
  4. Non-invasive optical imaging of neuropathology in vivo
    Brian Bacskai; Fiscal Year: 2009
  5. Anti-oxidant therapy in Alzheimer's disease
    Brian Bacskai; Fiscal Year: 2009
  6. Anti-oxidant therapy in Alzheimer's disease
    Brian J Bacskai; Fiscal Year: 2010
  7. Multiphoton microscopy for in vivo neural imaging
    Brian J Bacskai; Fiscal Year: 2010
  8. Anti-oxidant therapy in Alzheimer's disease
    Brian Bacskai; Fiscal Year: 2007
  9. Multiphoton microscopy for in vivo neural imaging.
    Brian Bacskai; Fiscal Year: 2006
  10. Non-invasive optical imaging of neuropathology in vivo
    Brian Bacskai; Fiscal Year: 2006

Collaborators

Detail Information

Publications58

  1. pmc Ultrasound enhanced delivery of molecular imaging and therapeutic agents in Alzheimer's disease mouse models
    Scott B Raymond
    The Harvard MIT Division of Health Sciences and Technology, Cambridge, Massachusetts, United States of America
    PLoS ONE 3:e2175. 2008
    ..Furthermore, this technique may be used to deliver a wide variety of small and large molecules to the brain for imaging and therapy in other neurodegenerative diseases...
  2. ncbi request reprint Fluorescence resonance energy transfer determinations using multiphoton fluorescence lifetime imaging microscopy to characterize amyloid-beta plaques
    Brian J Bacskai
    Massachusetts General Hospital, Department of Neurology Alzheimer s Disease Research Laboratory, 114 16th Street, Charlestown, Massachusetts 02129, USA
    J Biomed Opt 8:368-75. 2003
    ..Together these results demonstrate that FLIM allows sensitive measurements of protein-protein interactions on a spatial scale less than 10 nm using commercially available components...
  3. pmc Cerebrovascular lesions induce transient β-amyloid deposition
    Monica Garcia-Alloza
    Alzheimer Research Unit, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, 114 16th Street, Charlestown, MA 02129, USA
    Brain 134:3697-707. 2011
    ..Additionally, this study indicates that focal ischaemia provides an experimental paradigm in which to study the mechanisms of plaque seeding and growth...
  4. 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...
  5. pmc Four-dimensional multiphoton imaging of brain entry, amyloid binding, and clearance of an amyloid-beta ligand in transgenic mice
    Brian J Bacskai
    Department of Neurology Alzheimer s Disease Research Laboratory, Massachusetts General Hospital, 114 16th Street, Charlestown, MA 02129, USA
    Proc Natl Acad Sci U S A 100:12462-7. 2003
    ..WT mice showed rapid brain entry and clearance of PIB without any binding. These results demonstrate that the compound PIB has the properties required for a good amyloid-imaging agent in humans with or at risk for AD...
  6. pmc Existing plaques and neuritic abnormalities in APP:PS1 mice are not affected by administration of the gamma-secretase inhibitor LY-411575
    Monica Garcia-Alloza
    MassGeneral Institute for Neurodegenerative Diseases, Massachusetts General Hospital, 114 16th Street, Charlestown, MA 02129, USA
    Mol Neurodegener 4:19. 2009
    ..Therefore, a combination therapy of Abeta suppression with agents that increase clearance of amyloid and/or prevent neurotoxicity might be needed for a more effective treatment in patients with pre-existing pathology...
  7. ncbi request reprint Reversible memory loss in a mouse transgenic model of Alzheimer's disease
    Linda A Kotilinek
    Department of Neurology, University of Minnesota, Minneapolis 55455, USA
    J Neurosci 22:6331-5. 2002
    ..If these Abeta assemblies contribute significantly to memory loss in AD, then successfully targeting them might improve memory in some AD patients...
  8. pmc Differential effect of three-repeat and four-repeat tau on mitochondrial axonal transport
    Will Stoothoff
    MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA
    J Neurochem 111:417-27. 2009
    ..Our results indicate that tau-induced changes in axonal transport may be an underlying theme in neurodegenerative diseases associated with isoform specific changes in tau's interaction with microtubules...
  9. ncbi request reprint Preclinical characterization of amyloid imaging probes with multiphoton microscopy
    Jesse Skoch
    MassGeneral Institute for Neurodegenerative Disease, Department of Neurology Alzheimer s Disease Research Laboratory, Massachusetts General Hospital, 114 16th Street, Charlestown, MA 02129, USA
    J Alzheimers Dis 9:401-7. 2006
    ....
  10. ncbi request reprint Multiphoton imaging of ultrasound/Optison mediated cerebrovascular effects in vivo
    Scott B Raymond
    Harvard Biophysics Program, Harvard University, Boston, Massachusetts, USA
    J Cereb Blood Flow Metab 27:393-403. 2007
    ..These data corroborated previous studies suggesting increased endothelial transcytosis and breached tight junctions and demonstrated vasoconstriction, which might alter BBB permeability by modifying cerebral blood flow...
  11. pmc Rapid appearance and local toxicity of amyloid-beta plaques in a mouse model of Alzheimer's disease
    Melanie Meyer-Luehmann
    Alzheimer s Disease Research Laboratory, Department of Neurology, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA
    Nature 451:720-4. 2008
    ..Progressive neuritic changes ensue, leading to increasingly dysmorphic neurites over the next days to weeks. These data establish plaques as a critical mediator of neuritic pathology...
  12. ncbi request reprint Kinetics of cerebral amyloid angiopathy progression in a transgenic mouse model of Alzheimer disease
    Elissa M Robbins
    MassGeneral Institute for Neurodegenerative Disease, Department of Neurology, Massachusetts General Hospital, Charlestown, Massachusetts 02129, USA
    J Neurosci 26:365-71. 2006
    ..35% of total available vessel area per day (95% confidence interval, 0.3-0.4%). The consistent rate of disease progression implies that this model is amenable to investigations of therapeutic interventions...
  13. ncbi request reprint Amyloid precursor protein associates with a nicastrin-dependent docking site on the presenilin 1-gamma-secretase complex in cells demonstrated by fluorescence lifetime imaging
    Oksana Berezovska
    Alzheimer s Disease Research Laboratory, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA
    J Neurosci 23:4560-6. 2003
    ..We interpret these results to suggest that there is a noncatalytic docking site closely associated with PS1-gamma-secretase...
  14. ncbi request reprint In vivo optical imaging of amyloid aggregates in brain: design of fluorescent markers
    Evgueni E Nesterov
    Department of Chemistry and Institute for Soldier Nanotechnologies, Massachusetts Institute of Technology, Cambridge, MA 02139, USA
    Angew Chem Int Ed Engl 44:5452-6. 2005
  15. ncbi request reprint Progression of cerebral amyloid angiopathy in transgenic mouse models of Alzheimer disease
    Sarah B Domnitz
    Alzheimer Research Unit, Massachusetts General Institute for Neurodegenerative Disease, Massachusetts General Hospital, Charlestown, Massachusetts 02129, USA
    J Neuropathol Exp Neurol 64:588-94. 2005
    ..This approach should lead to more informed analysis of the consequences of evolving therapeutic options for AD on this related form of vascular pathology...
  16. ncbi request reprint Effects of apoE isoforms on beta-amyloid-induced matrix metalloproteinase-9 in rat astrocytes
    Shuzhen Guo
    Department of Neurology, Mass General Hospital, Charlestown, MA, USA
    Brain Res 1111:222-6. 2006
    ..Reduction of astrocytic MMP-9 by apoE4 may affect Abeta clearance and promote Abeta deposition in AD...
  17. ncbi request reprint Characterization of amyloid deposition in the APPswe/PS1dE9 mouse model of Alzheimer disease
    Monica Garcia-Alloza
    Alzheimer Research Unit, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, 114 16th Street, Charlestown, MA 02129, USA
    Neurobiol Dis 24:516-24. 2006
    ....
  18. ncbi request reprint Plaque-derived oxidative stress mediates distorted neurite trajectories in the Alzheimer mouse model
    Monica Garcia-Alloza
    Department of Neurology Alzheimer s Disease Research Laboratory, Massachusetts General Hospital, Charlestown, Massachusetts 02129, USA
    J Neuropathol Exp Neurol 65:1082-9. 2006
    ..The quantitative ex vivo screen combined with in vivo monitoring of efficacy should lead to more effective clinical therapies for the prevention of oxidative stress and neurotoxicity in AD...
  19. ncbi request reprint Age-dependent cerebrovascular dysfunction in a transgenic mouse model of cerebral amyloid angiopathy
    Hwa Kyoung Shin
    Stroke and Neurovascular Regulation Laboratory, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA
    Brain 130:2310-9. 2007
    ..These responses do not differ from controls when studied non-invasively prior to vascular Abeta deposition, thus challenging the view that elevated soluble Abeta levels are sufficient to cause cerebrovascular dysfunction...
  20. pmc Impaired spine stability underlies plaque-related spine loss in an Alzheimer's disease mouse model
    Tara L Spires-Jones
    MassGeneral Institute for Neurodegenerative Disease, Department of Neurology, Massachusetts General Hospital Harvard Medical School, Charlestown, Massachusetts, USA
    Am J Pathol 171:1304-11. 2007
    ..These data show a small population of rapidly changing spines in adult and even elderly mouse cortex; further, in the vicinity of amyloid plaques, spine stability is markedly impaired leading to loss of synaptic structural integrity...
  21. pmc A limited role for microglia in antibody mediated plaque clearance in APP mice
    Monica Garcia-Alloza
    Massachusetts General Hospital, Department of Neurology Alzheimer s Disease Research Laboratory, 114 16th Street, 2010, Charlestown, MA 02129, USA
    Neurobiol Dis 28:286-92. 2007
    ....
  22. doi request reprint Smart optical probes for near-infrared fluorescence imaging of Alzheimer's disease pathology
    Scott B Raymond
    Alzheimer s Disease Research Unit, Department of Neurology, Massachusetts General Hospital, 114 16th Street, Charlestown, MA 02129, USA
    Eur J Nucl Med Mol Imaging 35:S93-8. 2008
    ..However, Abeta-targeted optical probes often suffer from poor specificity and slow clearance from the brain. We are designing smart optical probes that emit characteristic fluorescence signal only when bound to Abeta...
  23. pmc Abeta plaques lead to aberrant regulation of calcium homeostasis in vivo resulting in structural and functional disruption of neuronal networks
    KISHORE V KUCHIBHOTLA
    Massachusetts General Hospital, Department of Neurology Alzheimer s Disease Research Laboratory, 114 16th Street, Charlestown, MA 02129, USA
    Neuron 59:214-25. 2008
    ..Together, these data demonstrate that senile plaques impair neuritic calcium homeostasis in vivo and result in the structural and functional disruption of neuronal networks...
  24. ncbi request reprint Bringing amyloid into focus
    Todd E Golde
    Nat Biotechnol 23:552-4. 2005
  25. ncbi request reprint Development of an optical approach for noninvasive imaging of Alzheimer's disease pathology
    Jesse Skoch
    Massachusetts General Hospital, MassGeneral Institute for Neurodegenerative Disease, Department of Neurology Alzheimer s Disease Research Unit, 114 16th Street, Charlestown, Massachusetts 02129, USA
    J Biomed Opt 10:11007. 2005
    ..Successful development of an optical detection platform would enable inexpensive, accessible, nonradioactive detection of the A beta deposits found in AD...
  26. ncbi request reprint A lipophilic thioflavin-T derivative for positron emission tomography (PET) imaging of amyloid in brain
    Chester A Mathis
    PET Facility, Department of Radiology, University of Pittsburgh, PA 15213, USA
    Bioorg Med Chem Lett 12:295-8. 2002
    ..Amyloid deposits were imaged with multiphoton microscopy in the brains of living transgenic mice following the systemic injection of unlabeled 6. [(11)C]6 is a promising amyloid imaging agent for Alzheimer's disease...
  27. ncbi request reprint Amyloid-beta antibody treatment leads to rapid normalization of plaque-induced neuritic alterations
    Julianne A Lombardo
    Center for Aging, Genetics, and Neurodegeneration, Department of Neurology, Massachusetts General Hospital, Charlestown, Massachusetts 02129, USA
    J Neurosci 23:10879-83. 2003
    ..Moreover, the rapid normalization of neuritic dystrophy suggests an unexpected degree of plasticity in the adult nervous system...
  28. ncbi request reprint Activated Notch1 associates with a presenilin-1/gamma-secretase docking site
    Pavan Ramdya
    Alzheimer s Research Unit, Massachusetts General Hospital, Charlestown, Massachusetts 02129, USA
    J Neurochem 87:843-50. 2003
    ..These results suggest a novel mechanism of ligand binding-mediated signal transduction of Notch1...
  29. ncbi request reprint Dysferlin interacts with annexins A1 and A2 and mediates sarcolemmal wound-healing
    Niall J Lennon
    Day Neuromuscular Research Laboratory, Massachusetts General Hospital, Charlestown, Massachusetts 02129, USA
    J Biol Chem 278:50466-73. 2003
    ..We propose a model of muscle membrane healing mediated by dysferlin that is relevant to both normal and dystrophic muscle and defines the annexins as potential muscular dystrophy genes...
  30. ncbi request reprint Monitoring proteins in intact cells
    Oksana Berezovska
    Alzheimer s Disease Research Laboratory, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA
    Sci Aging Knowledge Environ 2003:PE14. 2003
    ..This approach may have widespread applicability in studies of neurodegenerative disease mechanisms...
  31. ncbi request reprint In vivo imaging of reactive oxygen species specifically associated with thioflavine S-positive amyloid plaques by multiphoton microscopy
    Megan E McLellan
    Massachusetts General Hospital, Department of Neurology Alzheimer s Disease Research Laboratory, Charlestown, Massachusetts 02129, USA
    J Neurosci 23:2212-7. 2003
    ..Antioxidant therapy neutralizes these highly reactive molecules and may therefore be of therapeutic value in Alzheimer's disease...
  32. ncbi request reprint Alzheimer's disease: what multiphoton microscopy teaches us
    Brian J Bacskai
    Alzheimer s Disease Research Laboratory, Massachusetts General Hospital, Charlestown 02129, USA
    Neuroscientist 8:386-90. 2002
    ..This in vivo imaging approach allows direct examination of the natural history of plaques and evaluation of antiplaque therapeutics in mouse models of the disease...
  33. ncbi request reprint Imaging Abeta plaques in living transgenic mice with multiphoton microscopy and methoxy-X04, a systemically administered Congo red derivative
    William E Klunk
    Department of Psychiatry, University of Pittsburgh School of Medicine, Pennsylvania 15213, USA
    J Neuropathol Exp Neurol 61:797-805. 2002
    ....
  34. ncbi request reprint Non-Fc-mediated mechanisms are involved in clearance of amyloid-beta in vivo by immunotherapy
    Brian J Bacskai
    Alzheimer s Disease Research Laboratory, Massachusetts General Hospital, Charlestown, Massachusetts 02129, USA
    J Neurosci 22:7873-8. 2002
    ..Together, these results indicate that clearance of amyloid deposits in vivo may involve, in addition to Fc-dependent clearance, a non-Fc-mediated disruption of plaque structure...
  35. ncbi request reprint Imaging amyloid-beta deposits in vivo
    Brian J Bacskai
    Alzheimer Research Unit, Massachusetts General Hospital, Charlestown 02129, USA
    J Cereb Blood Flow Metab 22:1035-41. 2002
    ..This review describes the progress in developing reagents suitable for in vivo imaging of senile plaques...
  36. ncbi request reprint Imaging the pathology of Alzheimer's disease: amyloid-imaging with positron emission tomography
    William E Klunk
    Laboratory of Molecular Neuropharmacology, Department of Psychiatry, University of Pittsburgh School of Medicine, 705 Parran Hall, Pittsburgh, PA 15213, USA
    Neuroimaging Clin N Am 13:781-9, ix. 2003
    ..The capability to use positron emission tomography and selective markers for amyloid protein deposition promises to substantially alter the way we diagnosis and manage patients who have AD...
  37. ncbi request reprint The low density lipoprotein receptor-related protein (LRP) is a novel beta-secretase (BACE1) substrate
    Christine A F von Arnim
    Alzheimer Disease Research Laboratory, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA
    J Biol Chem 280:17777-85. 2005
    ..Taken together, these data suggest that there is a close interaction between BACE and LRP on the cell surface, and that LRP is a novel BACE substrate...
  38. ncbi request reprint Cortical synaptic integration in vivo is disrupted by amyloid-beta plaques
    Edward A Stern
    MassGeneral Institute for Neurodegenerative Disease, Department of Neurology, Massachusetts General Hospital, Charlestown, Massachusetts 02129, USA
    J Neurosci 24:4535-40. 2004
    ..Our results show that plaques disrupt the synchrony of convergent inputs, reducing the ability of neurons to successfully integrate and propagate information...
  39. pmc Dendritic spine abnormalities in amyloid precursor protein transgenic mice demonstrated by gene transfer and intravital multiphoton microscopy
    Tara L Spires
    Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA
    J Neurosci 25:7278-87. 2005
    ..Decreased spine density will likely contribute to altered neural system function and behavioral impairments observed in Tg2576 mice...
  40. pmc Anti-Abeta antibody treatment promotes the rapid recovery of amyloid-associated neuritic dystrophy in PDAPP transgenic mice
    Robert P Brendza
    Department of Neurology and Hope Center for Neurological Disorders, Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Clin Invest 115:428-33. 2005
    ..This analysis suggests that ongoing axonal and dendritic damage is secondary to Abeta and is, in part, rapidly reversible...
  41. ncbi request reprint Amyotrophic lateral sclerosis-associated SOD1 mutant proteins bind and aggregate with Bcl-2 in spinal cord mitochondria
    Piera Pasinelli
    Day Laboratory for Neuromuscular Research, Department of Neurology, Harvard Medical School, Mass General Institute for Neurodegenerative Disease, Massachusetts General Hospital, Charlestown, MA 02129, USA
    Neuron 43:19-30. 2004
    ..These findings provide new insights into the anti-apoptotic function of SOD1 and suggest that entrapment of Bcl-2 by large SOD1 aggregates may deplete motor neurons of this anti-apoptotic protein...
  42. ncbi request reprint Nonsteroidal anti-inflammatory drugs lower Abeta42 and change presenilin 1 conformation
    Alberto Lleo
    Alzheimer Research Unit, Massachusetts General Hospital, 114 16th St, Charlestown, Massachusetts 02129, USA
    Nat Med 10:1065-6. 2004
    ....
  43. ncbi request reprint Familial Alzheimer's disease presenilin 1 mutations cause alterations in the conformation of presenilin and interactions with amyloid precursor protein
    Oksana Berezovska
    Alzheimer Research Unit, Massachusetts General Hospital, Charlestown, Massachusetts 02129, USA
    J Neurosci 25:3009-17. 2005
    ..We propose that the conformational change we observed may therefore provide a shared molecular mechanism for FAD pathogenesis caused by a wide range of PS1 mutations...
  44. ncbi request reprint Techniques for brain imaging in vivo
    Monica Garcia-Alloza
    Massachusetts General Hospital, Department of Neurology Alzheimer s Disease Research Laboratory 114 16th Street, Charlestown, MA 02129, USA
    Neuromolecular Med 6:65-78. 2004
    ....
  45. pmc Comparison of frequency-domain and time-domain fluorescence lifetime tomography
    Anand T N Kumar
    Athinoula A Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA
    Opt Lett 33:470-2. 2008
    ..We also demonstrate experimentally, using complex-shaped phantoms, the advantages of the asymptotic time-domain approach over a Fourier-based approach for analyzing time-domain fluorescence data...
  46. pmc Detection of myelination using a novel histological probe
    Zhongmin Xiang
    The MassGeneral Institute for Neurodegenerative Diseases MIND, Charlestown, MA 02129 4404, USA
    J Histochem Cytochem 53:1511-6. 2005
    ..These dyes have been used successfully to detect normal myelin structure and myelin loss in a mouse model of demyelination disease...
  47. pmc A time domain fluorescence tomography system for small animal imaging
    Anand T N Kumar
    Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129, USA
    IEEE Trans Med Imaging 27:1152-63. 2008
    ..These results suggest the practical feasibility and advantages of a time domain approach for whole body small animal fluorescence molecular imaging, particularly with the use of lifetime as a contrast mechanism...
  48. ncbi request reprint In vivo imaging of amyloid-beta deposits in mouse brain with multiphoton microscopy
    Jesse Skoch
    Department of Neurology, Massachusetts General Hospital, Charlestown, MA, USA
    Methods Mol Biol 299:349-63. 2005
    ..The ability to monitor these hallmarks of Alzheimer's disease enables studies aimed at evaluating the efficacy of treatment and prevention strategies...
  49. pmc Physical and functional connection between auxilin and dynamin during endocytosis
    Sanja Sever
    Renal Unit, Nephrology Division, Department of Medicine, Harvard Medical School and Massachusetts General Hospital, Charlestown, MA 02129, USA
    EMBO J 25:4163-74. 2006
    ..Together, our findings support the model that the GTP-bound conformation of dynamin tetramers stimulates formation of constricted coated pits at the plasma membrane by regulating the chaperone activity of hsc70/auxilin...
  50. doi request reprint In vivo imaging reveals dissociation between caspase activation and acute neuronal death in tangle-bearing neurons
    Tara L Spires-Jones
    MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA
    J Neurosci 28:862-7. 2008
    ....
  51. ncbi request reprint Fluorescence-lifetime-based tomography for turbid media
    Anand T N Kumar
    Athinoula A Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA
    Opt Lett 30:3347-9. 2005
    ....
  52. pmc CysLT2 receptors interact with CysLT1 receptors and down-modulate cysteinyl leukotriene dependent mitogenic responses of mast cells
    Yongfeng Jiang
    Department of Medicine, Harvard Medical School, Boston, MA, USA
    Blood 110:3263-70. 2007
    ..Negative regulation of CysLT(1)-induced mitogenic signaling responses of MCs by CysLT(2) demonstrates physiologically relevant functions for GPCR heterodimers on primary cells central to inflammation...
  53. ncbi request reprint Assays and functional properties of auxilin-dynamin interactions
    Sanja Sever
    Department of Medicine, Harvard Medical School, Boston, Massachusetts, USA
    Methods Enzymol 404:570-85. 2005
    ..Here we describe three different in vitro assays that monitor auxilin-dynamin interactions, as well as fluorescence lifetime imaging microscopy that identify direct interactions between dynamin and auxilin in cells...
  54. ncbi request reprint Modular design for in vivo optical imaging and ultrasound treatment in the murine brain
    Scott B Raymond
    IEEE Trans Ultrason Ferroelectr Freq Control 54:431-4. 2007
    ..Ultrasound components are integrated into a commercial multiphoton microscope, and animals are imaged during ultrasound-induced blood-brain barrier disruption...
  55. pmc Depth-resolved optical imaging and microscopy of vascular compartment dynamics during somatosensory stimulation
    Elizabeth M C Hillman
    Athinoula A Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Building 149, 13th Street, Charlestown, MA 02129, USA
    Neuroimage 35:89-104. 2007
    ....
  56. ncbi request reprint Time-domain fluorescent plate reader for cell based protein-protein interaction and protein conformation assays
    Phill B Jones
    Athinoula A Martinos Center for Biomedical Imaging, Harvard Medical School, Massachusetts General Hospital, 149 13th Street, Charlestown, Massachusetts 02129, USA
    J Biomed Opt 11:054024. 2006
    ..Presenilin 1 (PS1) is known to be important in Amyloid Precursor Protein (APP) processing in Alzheimer's disease. Using transfected cells, we demonstrate APP-PS1 interactions by FRET in a cell-based, 96-well plate format...
  57. pmc The membrane organization of leukotriene synthesis
    Asim K Mandal
    Department of Medicine, Massachusetts General Hospital, 149 The Navy Yard, 13th Street, Charlestown, MA 02129, USA
    Proc Natl Acad Sci U S A 101:6587-92. 2004
    ..The results indicate that the formation of LTC(4) and LTB(4) may be determined by the compartmentalization of biosynthetic enzymes in discrete molecular complexes...
  58. ncbi request reprint Antibody-mediated clearance of amyloid-beta peptide from cerebral amyloid angiopathy revealed by quantitative in vivo imaging
    Claudia M Prada
    Department of Neurology Alzheimer Research Unit, Massachusetts General Hospital, Charlestown, Massachusetts 02129, USA
    J Neurosci 27:1973-80. 2007
    ..This quantitative in vivo imaging approach directly demonstrates that CAA in a transgenic mouse model can be cleared with an optimized immunotherapy...

Research Grants23

  1. Non-invasive optical imaging of neuropathology in vivo
    Brian Bacskai; Fiscal Year: 2007
    ..Principal investigator Brian Bacskai at MGH has extensive experience in optical imaging, in vivo detection of neuropathology and biomedical ..
  2. Mechanisms of amyloid-beta clearance.
    Brian Bacskai; Fiscal Year: 2003
    ..We will test whether they are disaggregating agents in vivo. The results will strongly impact the development of treatments aimed at removing senile plaques and the associated neurological damage in Alzheimer's disease. ..
  3. Mechanisms of amyloid-beta clearance.
    Brian Bacskai; Fiscal Year: 2006
    ..We will test whether they are disaggregating agents in vivo. The results will strongly impact the development of treatments aimed at removing senile plaques and the associated neurological damage in Alzheimer's disease. ..
  4. Non-invasive optical imaging of neuropathology in vivo
    Brian Bacskai; Fiscal Year: 2009
    ..Principal investigator Brian Bacskai at MGH has extensive experience in optical imaging, in vivo detection of neuropathology and biomedical ..
  5. Anti-oxidant therapy in Alzheimer's disease
    Brian Bacskai; Fiscal Year: 2009
    ..abstract_text> ..
  6. Anti-oxidant therapy in Alzheimer's disease
    Brian J Bacskai; Fiscal Year: 2010
    ..abstract_text> ..
  7. Multiphoton microscopy for in vivo neural imaging
    Brian J Bacskai; Fiscal Year: 2010
    ..All together, these technological advances will support in vivo cellular imaging as a platform to understand brain function and treat neurological diseases. ..
  8. Anti-oxidant therapy in Alzheimer's disease
    Brian Bacskai; Fiscal Year: 2007
    ....
  9. Multiphoton microscopy for in vivo neural imaging.
    Brian Bacskai; Fiscal Year: 2006
    ..In summary, the proposals outlined in this application will lead to generally applicable new techniques for cellular and molecular imaging in the intact brain. ..
  10. Non-invasive optical imaging of neuropathology in vivo
    Brian Bacskai; Fiscal Year: 2006
    ..Principal investigator Brian Bacskai at MGH has extensive experience in optical imaging, in vivo detection of neuropathology and biomedical ..
  11. Anti-oxidant therapy in Alzheimer's disease
    Brian Bacskai; Fiscal Year: 2006
    ....
  12. Multiphoton microscopy for in vivo neural imaging.
    Brian Bacskai; Fiscal Year: 2005
    ..In summary, the proposals outlined in this application will lead to generally applicable new techniques for cellular and molecular imaging in the intact brain. ..
  13. Multiphoton microscopy for in vivo neural imaging.
    Brian Bacskai; Fiscal Year: 2002
    ..In summary, the proposals outlined in this application will lead to generally applicable new techniques for cellular and molecular imaging in the intact brain. ..
  14. Multiphoton microscopy for in vivo neural imaging.
    Brian Bacskai; Fiscal Year: 2003
    ..In summary, the proposals outlined in this application will lead to generally applicable new techniques for cellular and molecular imaging in the intact brain. ..
  15. Multiphoton microscopy for in vivo neural imaging
    Brian Bacskai; Fiscal Year: 2009
    ..All together, these technological advances will support in vivo cellular imaging as a platform to understand brain function and treat neurological diseases. ..
  16. Multiphoton microscopy for in vivo neural imaging.
    Brian Bacskai; Fiscal Year: 2004
    ..In summary, the proposals outlined in this application will lead to generally applicable new techniques for cellular and molecular imaging in the intact brain. ..
  17. Multiphoton microscopy for in vivo neural imaging
    Brian Bacskai; Fiscal Year: 2007
    ..All together, these technological advances will support in vivo cellular imaging as a platform to understand brain function and treat neurological diseases. ..
  18. Non-invasive optical imaging of neuropathology in vivo
    Brian J Bacskai; Fiscal Year: 2010
    ..Principal investigator Brian Bacskai at MGH has extensive experience in optical imaging, in vivo detection of neuropathology and biomedical ..