senile plaques

Summary

Summary: Spherical masses consisting of amyloid fibrils and neuronal processes.

Top Publications

  1. pmc Oligomeric amyloid beta associates with postsynaptic densities and correlates with excitatory synapse loss near senile plaques
    Robert M Koffie
    Neurology Department, Massachusetts General Hospital, Charlestown, MA 02129, USA
    Proc Natl Acad Sci U S A 106:4012-7. 2009
  2. ncbi Peripherally administered antibodies against amyloid beta-peptide enter the central nervous system and reduce pathology in a mouse model of Alzheimer disease
    F Bard
    Elan Pharmaceuticals, 800 Gateway Boulevard, South San Francisco, California 94080, USA
    Nat Med 6:916-9. 2000
  3. ncbi Enhanced proteolysis of beta-amyloid in APP transgenic mice prevents plaque formation, secondary pathology, and premature death
    Malcolm A Leissring
    Center for Neurologic Diseases, Department of Neurology, Brigham and Women s Hospital, Harvard Medical School, Harvard Medical School, Boston, MA 02115, USA
    Neuron 40:1087-93. 2003
  4. ncbi Intracellular amyloid-beta in Alzheimer's disease
    Frank M LaFerla
    Department of Neurobiology and Behaviour, and Institute for Brain Aging and Dementia, University of California, Irvine, California 92697 4545, USA
    Nat Rev Neurosci 8:499-509. 2007
  5. ncbi Neuropathologic features of amnestic mild cognitive impairment
    Ronald C Petersen
    Alzheimer s Disease Research Center and Department of Neurology, Mayo Clinic College of Medicine, 200 First Street SW, Rochester, MN 55905, USA
    Arch Neurol 63:665-72. 2006
  6. ncbi Antiamyloidogenic and neuroprotective functions of cathepsin B: implications for Alzheimer's disease
    Sarah Mueller-Steiner
    Gladstone Institute of Neurological Disease, University of California, San Francisco, 1650 Owens Street, 94158, USA
    Neuron 51:703-14. 2006
  7. ncbi Mitochondrial degeneration in dystrophic neurites of senile plaques may lead to extracellular deposition of fine filaments
    John C Fiala
    Department of Health Sciences, Boston University, 635 Commonwealth Ave, Boston, MA 02215, USA
    Brain Struct Funct 212:195-207. 2007
  8. pmc Detection of neuritic plaques in Alzheimer's disease by magnetic resonance microscopy
    H Benveniste
    Department of Radiology, Duke University Medical Center, Durham, NC 27710, USA
    Proc Natl Acad Sci U S A 96:14079-84. 1999
  9. ncbi The microglial phagocytic role with specific plaque types in the Alzheimer disease brain
    Michael R D'Andrea
    Drug Discovery, Johnson and Johnson Pharmaceutical Research and Development, D404, Spring House, PA 19477, USA
    Neurobiol Aging 25:675-83. 2004
  10. ncbi Hematopoietic prostaglandin D synthase and DP1 receptor are selectively upregulated in microglia and astrocytes within senile plaques from human patients and in a mouse model of Alzheimer disease
    Ikuko Mohri
    FrDepartment of Mental Health and Environmental Effects Research, The Research Center for Child Mental Development, Osaka University Graduate School of Medicine, Suita, Osaka, Japan
    J Neuropathol Exp Neurol 66:469-80. 2007

Research Grants

  1. Statin modulation of immunotherapy for Alzheimer disease
    Jun Tan; Fiscal Year: 2012
  2. Zhongcong Xie; Fiscal Year: 2016
  3. Glucose Metabolic, Amyloid, and Tau Brain Imaging in Down's Syndrome and Dementia
    GARY WILLIAM SMALL; Fiscal Year: 2013
  4. Extracellular Zinc Buffering and A-beta Oligomerization
    GUIDO FAAS; Fiscal Year: 2012
  5. Bernard G Schreurs; Fiscal Year: 2015
  6. Andrea Joan Tenner; Fiscal Year: 2014
  7. Huaxi Xu; Fiscal Year: 2016
  8. Beta-Amyloid Immunization in a Canine Model of Aging
    Elizabeth Head; Fiscal Year: 2013
  9. AMYLOID PLAQUE AND TANGLE IMAGING IN AGING AND DEMENTIA
    GARY WILLIAM SMALL; Fiscal Year: 2010
  10. Cyclohexanehexol Therapy in Transgenic Models of Alzheimer's Disease
    Alpaslan Dedeoglu; Fiscal Year: 2013

Detail Information

Publications289 found, 100 shown here

  1. pmc Oligomeric amyloid beta associates with postsynaptic densities and correlates with excitatory synapse loss near senile plaques
    Robert M Koffie
    Neurology Department, Massachusetts General Hospital, Charlestown, MA 02129, USA
    Proc Natl Acad Sci U S A 106:4012-7. 2009
    ..a cognitive decline in Alzheimer's disease (AD), but whether this is caused by fibrillar deposits known as senile plaques or soluble oligomeric forms of amyloid beta (Abeta) is controversial...
  2. ncbi Peripherally administered antibodies against amyloid beta-peptide enter the central nervous system and reduce pathology in a mouse model of Alzheimer disease
    F Bard
    Elan Pharmaceuticals, 800 Gateway Boulevard, South San Francisco, California 94080, USA
    Nat Med 6:916-9. 2000
    ....
  3. ncbi Enhanced proteolysis of beta-amyloid in APP transgenic mice prevents plaque formation, secondary pathology, and premature death
    Malcolm A Leissring
    Center for Neurologic Diseases, Department of Neurology, Brigham and Women s Hospital, Harvard Medical School, Harvard Medical School, Boston, MA 02115, USA
    Neuron 40:1087-93. 2003
    ..Our findings demonstrate that chronic upregulation of Abeta-degrading proteases represents an efficacious therapeutic approach to combating Alzheimer-type pathology in vivo...
  4. ncbi Intracellular amyloid-beta in Alzheimer's disease
    Frank M LaFerla
    Department of Neurobiology and Behaviour, and Institute for Brain Aging and Dementia, University of California, Irvine, California 92697 4545, USA
    Nat Rev Neurosci 8:499-509. 2007
    ....
  5. ncbi Neuropathologic features of amnestic mild cognitive impairment
    Ronald C Petersen
    Alzheimer s Disease Research Center and Department of Neurology, Mayo Clinic College of Medicine, 200 First Street SW, Rochester, MN 55905, USA
    Arch Neurol 63:665-72. 2006
    ..The neuropathologic substrate of amnestic mild cognitive impairment (aMCI) is not known...
  6. ncbi Antiamyloidogenic and neuroprotective functions of cathepsin B: implications for Alzheimer's disease
    Sarah Mueller-Steiner
    Gladstone Institute of Neurological Disease, University of California, San Francisco, 1650 Owens Street, 94158, USA
    Neuron 51:703-14. 2006
    ..Thus, CatB likely fulfills antiamyloidogenic and neuroprotective functions. Insufficient CatB activity might promote AD; increasing CatB activity could counteract the neuropathology of this disease...
  7. ncbi Mitochondrial degeneration in dystrophic neurites of senile plaques may lead to extracellular deposition of fine filaments
    John C Fiala
    Department of Health Sciences, Boston University, 635 Commonwealth Ave, Boston, MA 02215, USA
    Brain Struct Funct 212:195-207. 2007
    ..This progression of degeneration suggests that extracellular filaments originate inside degenerating mitochondria of neuritic diverticula, which may be a common process in diverse diseases...
  8. pmc Detection of neuritic plaques in Alzheimer's disease by magnetic resonance microscopy
    H Benveniste
    Department of Radiology, Duke University Medical Center, Durham, NC 27710, USA
    Proc Natl Acad Sci U S A 96:14079-84. 1999
    ..Clearly, the ability to detect and follow the early progression of amyloid-positive brain lesions will greatly aid and simplify the many possibilities to intervene pharmacologically in AD...
  9. ncbi The microglial phagocytic role with specific plaque types in the Alzheimer disease brain
    Michael R D'Andrea
    Drug Discovery, Johnson and Johnson Pharmaceutical Research and Development, D404, Spring House, PA 19477, USA
    Neurobiol Aging 25:675-83. 2004
    ..In summary, the data presented suggests that plaque associated microglial activation is typically subsequent to specific amyloid plaque formations in the AD brain...
  10. ncbi Hematopoietic prostaglandin D synthase and DP1 receptor are selectively upregulated in microglia and astrocytes within senile plaques from human patients and in a mouse model of Alzheimer disease
    Ikuko Mohri
    FrDepartment of Mental Health and Environmental Effects Research, The Research Center for Child Mental Development, Osaka University Graduate School of Medicine, Suita, Osaka, Japan
    J Neuropathol Exp Neurol 66:469-80. 2007
    ..Immunocytochemical analysis showed HPGDS expression to be localized in the microglia surrounding senile plaques. In situ hybridization studies revealed that DP1 mRNA was specifically localized in microglia and reactive ..
  11. ncbi Bone marrow-derived microglia play a critical role in restricting senile plaque formation in Alzheimer's disease
    Alain R Simard
    Laboratory of Molecular Endocrinology, CHUL Research Center and Department of Anatomy and Physiology, Laval University, 2705 Laurier Boul, Quebec G1V 4G2, Canada
    Neuron 49:489-502. 2006
    ..Therapeutic strategies aiming to improve their recruitment could potentially lead to a new powerful tool for the elimination of toxic senile plaques.
  12. doi Assessment of beta-amyloid in a frontal cortical brain biopsy specimen and by positron emission tomography with carbon 11-labeled Pittsburgh Compound B
    Ville Leinonen
    Department of Neurosurgery, Kuopio University Hospital, PO Box 1777, 70211 Kuopio, Finland
    Arch Neurol 65:1304-9. 2008
    ..To compare carbon 11-labeled Pittsburgh Compound B ([11C]PiB) positron emission tomography (PET) findings in patients with and without Alzheimer disease lesions in frontal cortical biopsy specimens...
  13. ncbi Localization of neurofibrillary tangles and beta-amyloid plaques in the brains of living patients with Alzheimer disease
    Kooresh Shoghi-Jadid
    Division of Nuclear Medicine, UCLA School of Medicine, Los Angeles, CA, USA
    Am J Geriatr Psychiatry 10:24-35. 2002
    ..emission tomography to determine the localization and load of neurofibrillary tangles (NFTs) and beta-amyloid senile plaques (APs) in the brains of living Alzheimer disease (AD) patients...
  14. ncbi In situ oxidative catalysis by neurofibrillary tangles and senile plaques in Alzheimer's disease: a central role for bound transition metals
    L M Sayre
    Department of Chemistry, Case Western Reserve University, Cleveland, Ohio 44106, USA
    J Neurochem 74:270-9. 2000
    ..In this study, using a novel in situ detection system, we show that neurofibrillary tangles and senile plaques are major sites for catalytic redox reactivity...
  15. ncbi Mild hypercholesterolemia is an early risk factor for the development of Alzheimer amyloid pathology
    M A Pappolla
    University of South Alabama, Mobile, USA
    Neurology 61:199-205. 2003
    ..Epidemiologic and experimental data suggest that cholesterol may play a role in the pathogenesis of AD. Modulation of cholesterolemia in transgenic animal models of AD strongly alters amyloid pathology...
  16. ncbi Amyloid-beta immunization effectively reduces amyloid deposition in FcRgamma-/- knock-out mice
    Pritam Das
    Department of Neuroscience, Mayo Clinic, Jacksonville, Florida 32224, USA
    J Neurosci 23:8532-8. 2003
    ..We conclude that after Abeta immunization, the effects of anti-Abeta antibodies on Abeta deposition in APP Tg2576 transgenic mice are not dependent on FcR-mediated phagocytic events...
  17. ncbi Activation of beta2-adrenergic receptor stimulates gamma-secretase activity and accelerates amyloid plaque formation
    Yanxiang Ni
    Laboratory of Molecular Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, China
    Nat Med 12:1390-6. 2006
    ..Thus, beta(2)-AR activation can stimulate gamma-secretase activity and amyloid plaque formation, which suggests that abnormal activation of beta(2)-AR might contribute to Abeta accumulation in Alzheimer disease pathogenesis...
  18. ncbi Absence of C1q leads to less neuropathology in transgenic mouse models of Alzheimer's disease
    Maria Isabel Fonseca
    Department of Molecular Biology and Biochemistry, University of California, Irvine, California 92697, USA
    J Neurosci 24:6457-65. 2004
    ....
  19. pmc In vivo visualization of Alzheimer's amyloid plaques by magnetic resonance imaging in transgenic mice without a contrast agent
    Clifford R Jack
    Department of Radiology, Mayo Clinic College of Medicine, Rochester, Minnesota 55905, USA
    Magn Reson Med 52:1263-71. 2004
    ..To our knowledge this work represents the first demonstration of noninvasive in vivo visualization of individual AD plaques without the use of a contrast agent...
  20. ncbi Visual association pathology in preclinical Alzheimer disease
    Ann C McKee
    Department of Neurology and Pathology, Boston University School of Medicine, Bedford Veterans Administration Medical Center, MA 01730, USA
    J Neuropathol Exp Neurol 65:621-30. 2006
    ..Dense AD pathology in area 19 is present in some cognitively intact subjects with preclinical AD. The unique metabolic, connectional, and vascular features of this region may confer enhanced vulnerability to neurodegeneration...
  21. ncbi Age-dependent changes in brain, CSF, and plasma amyloid (beta) protein in the Tg2576 transgenic mouse model of Alzheimer's disease
    T Kawarabayashi
    Mayo Clinic Jacksonville, Jacksonville, Florida 32224, USA
    J Neurosci 21:372-81. 2001
    ..If a similar decline occurs in human plasma, it is possible that measurement of plasma Abeta may be useful as a premorbid biomarker for AD...
  22. ncbi 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
    Transgenic (Tg) mouse models overexpressing amyloid precursor protein (APP) develop senile plaques similar to those found in Alzheimer's disease in an age-dependent manner...
  23. ncbi Aspirin and non-steroidal anti-inflammatory drugs inhibit amyloid-beta aggregation
    T Thomas
    Woodlands Medical Center and Endron Therapeutics, 3150 Tampa Road, 16 Oldsmar, FL 34677, USA
    Neuroreport 12:3263-7. 2001
    ..NSAIDS may have a role in the prevention and treatment of AD, in addition to a number of age-related disorders such as arthritis, cardiovascular disease and cancer...
  24. ncbi Frequency of stages of Alzheimer-related lesions in different age categories
    H Braak
    Department of Morphology, J W Goethe University, Frankfurt, Germany
    Neurobiol Aging 18:351-7. 1997
    ..The arithmetic means of the stages of both the amyloid-depositing and the neurofibrillary pathology increase with age. Age is a risk factor for Alzheimer's disease...
  25. pmc A non-toxic ligand for voxel-based MRI analysis of plaques in AD transgenic mice
    Einar M Sigurdsson
    Department of Psychiatry, New York University School of Medicine, New York, NY 10016, USA
    Neurobiol Aging 29:836-47. 2008
    ..3) Smaller, earlier plaques require contrast ligand for MRI visualization. Our ligand when combined with VBA may be useful for following therapeutic approaches targeting amyloid in transgenic mouse models...
  26. ncbi Formation of neurofibrillary tangles in P301l tau transgenic mice induced by Abeta 42 fibrils
    J Gotz
    Division of Psychiatry Research, University of Zurich, August Forel Strasse 1, 8008 Zurich, Switzerland
    Science 293:1491-5. 2001
    ..NFTs were composed of twisted filaments and occurred in 6-month-old mice as early as 18 days after Abeta42 injections. Our data support the hypothesis that Abeta42 fibrils can accelerate NFT formation in vivo...
  27. ncbi Regression stage senile plaques in the natural course of Alzheimer's disease
    T Oide
    Department of Laboratory Medicine, Musashi Hospital, National Center of Neurology and Psychiatry, Kodaira, Tokyo, Japan
    Neuropathol Appl Neurobiol 32:539-56. 2006
    ..We thus examined 24 autopsied AD brains. A novel form of senile plaques, termed 'remnant plaques', was identified...
  28. ncbi 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...
  29. ncbi 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
    ....
  30. ncbi PET of brain amyloid and tau in mild cognitive impairment
    Gary W Small
    Department of Psychiatry and Biobehavioral Sciences and the Semel Institute for Neuroscience and Human Behavior, David Geffen School of Medicine at the University of California, Los Angeles, USA
    N Engl J Med 355:2652-63. 2006
    Amyloid senile plaques and tau neurofibrillary tangles are neuropathological hallmarks of Alzheimer's disease that accumulate in the cortical regions of the brain in persons with mild cognitive impairment who are at risk for Alzheimer's ..
  31. ncbi Neuropathology of cognitively normal elderly
    D S Knopman
    Department of Neurology, Mayo Clinic and Mayo Foundation, Rochester, Minnesota 55905, USA
    J Neuropathol Exp Neurol 62:1087-95. 2003
    ..The few subjects with more severe AD pathology can be expected based on incidence rates of AD in the very elderly...
  32. ncbi Part of membrane-bound Abeta exists in rafts within senile plaques in Tg2576 mouse brain
    Hideko Kokubo
    Gunma University School of Health Sciences, 3 39 15 Showa Machi, 371 8514 Maebashi, Japan
    Neurobiol Aging 26:409-18. 2005
    ..After observing the exact areas of senile plaques by reflection contrast microscopy, we observed these same plaques under an electron microscope...
  33. ncbi The molecular biology of senile plaques and neurofibrillary tangles in Alzheimer's disease
    Richard A Armstrong
    Vision Sciences, Aston University, Birmingham B4 7ET, UK
    Folia Neuropathol 47:289-99. 2009
    Since the earliest descriptions of the disease, senile plaques (SP) and neurofibrillary tangles (NFT) have been regarded as the pathological 'hallmarks' of Alzheimer's disease (AD)...
  34. doi Demonstration of aluminum in amyloid fibers in the cores of senile plaques in the brains of patients with Alzheimer's disease
    Sakae Yumoto
    Yumoto Institute of Neurology, Kawadacho 6 11, Shinjuku ku, Tokyo 162 0054, Japan
    J Inorg Biochem 103:1579-84. 2009
    ..We identified senile plaques by observation using TEM and detected Al in amyloid fibers in the cores of senile plaques located in the ..
  35. doi What initiates the formation of senile plaques? The origin of Alzheimer-like dementias in capillary haemorrhages
    Jonathan Stone
    Discipline of Physiology, Bosch Institute and School of Medical Sciences, University of Sydney, Sydney, NSW, Australia
    Med Hypotheses 71:347-59. 2008
    ..Advances in the treatment of dementia will be gained from techniques that minimise the neural damage caused by a multitude of tiny strokes...
  36. ncbi The role of microglial cells and astrocytes in fibrillar plaque evolution in transgenic APP(SW) mice
    J Wegiel
    New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY, USA
    Neurobiol Aging 22:49-61. 2001
    ..Microglial cells appear to release large amounts of fibrillar Abeta and accumulate traces of fibrillar Abeta in a lysosomal pathway...
  37. pmc Linking Abeta and tau in late-onset Alzheimer's disease: a dual pathway hypothesis
    Scott A Small
    Taub Institute for Research on Alzheimer s Disease and the Aging Brain, Department of Neurology, Columbia University College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA
    Neuron 60:534-42. 2008
    ..This model may account for the results of recent drug trials and, if confirmed, may guide future drug development...
  38. ncbi Intraneuronal Abeta accumulation precedes plaque formation in beta-amyloid precursor protein and presenilin-1 double-transgenic mice
    O Wirths
    Department of Psychiatry, University of Bonn Medical Center, Sigmund-Freud-Strasse 25, 53105, Bonn, Germany
    Neurosci Lett 306:116-20. 2001
    ..Interestingly, intraneuronal Abeta staining was no longer detected in the brain of aged double-transgenic mice, which correlates with the typical neuropathology in the brain of chronic AD patients...
  39. ncbi Intraneuronal abeta-amyloid precedes development of amyloid plaques in Down syndrome
    K A Gyure
    Department of Neuropathy, Armed Forces Institute of Pathology, Washington, DC, USA
    Arch Pathol Lab Med 125:489-92. 2001
    ..OBJECTIVE: To study the development of amyloid deposits, senile plaques, astrocytic and microglial reactions, and neurofibrillary tangles in the brains of young individuals (<30 ..
  40. ncbi Interlaboratory comparison of assessments of Alzheimer disease-related lesions: a study of the BrainNet Europe Consortium
    Irina Alafuzoff
    Department of Neuroscience and Neurology, Kuopio University, Kuopio University Hospital, Finland
    J Neuropathol Exp Neurol 65:740-57. 2006
    ..Therefore, the IHC/HPtau methodology to visualize NFTs and neuropil threads should be considered as a method of choice in a future diagnostic protocol for Alzheimer disease...
  41. ncbi Transgenic mice overexpressing amyloid beta protein are an incomplete model of Alzheimer disease
    Claudia Schwab
    Kinsmen Laboratory of Neurological Research, Division of Neurology, University of British Columbia, Vancouver, BC, Canada V6T 1Z3
    Exp Neurol 188:52-64. 2004
    ..Therapeutic strategies for the treatment of AD based on tg mouse models that overexpress Abeta may be limited in their application...
  42. ncbi Targeting small Abeta oligomers: the solution to an Alzheimer's disease conundrum?
    W L Klein
    Northwestern University Institute for Neuroscience and Dept of Neurobiology and Physiology, Northwestern University, 2153 N Campus Drive, Evanston, IL 60208, USA
    Trends Neurosci 24:219-24. 2001
    ..disease (AD), self-aggregation of Abeta becomes rampant, manifested most strikingly as the amyloid fibrils of senile plaques. Because fibrils can kill neurons in culture, it has been argued that fibrils initiate the neurodegenerative ..
  43. ncbi High-level neuronal expression of abeta 1-42 in wild-type human amyloid protein precursor transgenic mice: synaptotoxicity without plaque formation
    L Mucke
    Gladstone Institute of Neurological Disease, Department of Neurology, and Neuroscience Program, University of California, San Francisco, California 94141 9100, USA
    J Neurosci 20:4050-8. 2000
    ..Our results support the emerging view that plaque-independent Abeta toxicity plays an important role in the development of synaptic deficits in AD and related conditions...
  44. ncbi Immune reactive cells in senile plaques and cognitive decline in Alzheimer's disease
    Anne K Vehmas
    Department of Pathology, Neuropathology Division, The Johns Hopkins University School of Medicine, 720 Rutland Avenue, Ross 558, Baltimore, MD 21205 2196, USA
    Neurobiol Aging 24:321-31. 2003
    ..Tau immunoreactivity appears as the strongest morphological correlate of dementia...
  45. doi Autoantibodies against beta-amyloid are common in Alzheimer's disease and help control plaque burden
    Alexander Kellner
    Institute of Neuropathology, University Medical Center Hamburg Eppendorf, Hamburg, Germany
    Ann Neurol 65:24-31. 2009
    ..Here, we investigate whether naturally occurring autoantibodies to beta-amyloid contribute to beta-amyloid plaque removal in nonimmunized AD patients...
  46. ncbi Microglial activation facilitates Abeta plaque removal following intracranial anti-Abeta antibody administration
    Donna M Wilcock
    Department of Pharmacology, Alzheimer s Research Laboratory, University of South Florida, Tampa, FL 33612, USA
    Neurobiol Dis 15:11-20. 2004
    ..These data suggest that microglial activation is necessary for efficient removal of compact amyloid deposits with immunotherapy. Inhibition of this activation may result in an impaired clinical response to vaccination against Abeta...
  47. ncbi Intracranially administered anti-Abeta antibodies reduce beta-amyloid deposition by mechanisms both independent of and associated with microglial activation
    Donna M Wilcock
    Department of Pharmacology, Alzheimer s Research Laboratory, University of South Florida, Tampa, Florida 33612, USA
    J Neurosci 23:3745-51. 2003
    ..The results are discussed in the context of other studies identifying coincident microglial activation and amyloid removal in APP transgenic animals...
  48. ncbi Disruption of corticocortical connections ameliorates amyloid burden in terminal fields in a transgenic model of Abeta amyloidosis
    Jin G Sheng
    Department of Pathology Division of Neuropathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    J Neurosci 22:9794-9. 2002
    ....
  49. ncbi A learning deficit related to age and beta-amyloid plaques in a mouse model of Alzheimer's disease
    G Chen
    Department of Neuroscience, University of Edinburgh, UK
    Nature 408:975-9. 2000
    ....
  50. ncbi Treatment with a copper-zinc chelator markedly and rapidly inhibits beta-amyloid accumulation in Alzheimer's disease transgenic mice
    R A Cherny
    Department of Pathology, The University of Melbourne and, The Mental Health Research Institute of Victoria, Australia
    Neuron 30:665-76. 2001
    ..General health and body weight parameters were significantly more stable in the treated animals. These results support targeting the interactions of Cu and Zn with Abeta as a novel therapy for the prevention and treatment of AD...
  51. ncbi 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 low density lipoprotein receptor-related protein (LRP) is a multifunctional receptor which is present on senile plaques in Alzheimer's disease (AD)...
  52. ncbi Prevention of age-related spatial memory deficits in a transgenic mouse model of Alzheimer's disease by chronic Ginkgo biloba treatment
    Robert W Stackman
    Department of Behavioral Neuroscience, Oregon Health and Science University, Portland, OR 97239 3098, USA
    Exp Neurol 184:510-20. 2003
    ..These data indicate that chronic Ginkgo biloba treatment can block an age-dependent decline in spatial cognition without altering Abeta levels and without suppressing protein oxidation in a transgenic mouse model of AD...
  53. ncbi Decreased neprilysin immunoreactivity in Alzheimer disease, but not in pathological aging
    Deng Shun Wang
    Department of Neuroscience, Mayo Clinic College of Medicine, 4500 San Pablo Road, Jacksonville, FL 32224, USA
    J Neuropathol Exp Neurol 64:378-85. 2005
    ..In contrast, both PA and AD had more senile plaques and Abeta1-42 than N. NEP immunoreactivity was decreased in AD but not in PA...
  54. pmc Cerebrovascular smooth muscle actin is increased in nondemented subjects with frequent senile plaques at autopsy: implications for the pathogenesis of Alzheimer disease
    Christine M Hulette
    Department of Pathology Neuropathology, Joseph and Kathleen Price Bryan Alzheimer Disease Research Center, Duke University Medical Center, Durham, NC, USA
    J Neuropathol Exp Neurol 68:417-24. 2009
    ..subjects without significant AD type pathology ("Normal"; n = 20), nondemented subjects with frequent senile plaques at autopsy ("Preclinical AD"; n = 20), and subjects with frontotemporal dementia ("FTD"; n = 10)...
  55. ncbi Nanoscale biogenic iron oxides and neurodegenerative disease
    J Dobson
    Centre for Science and Technology in Medicine, Department of Biomedical Engineering and Medical Physics, Keele University, Thornburrow Drive, Hartshill, Stroke on Trent ST4 7QB, UK
    FEBS Lett 496:1-5. 2001
    ..work indicates that nanoscale magnetic biominerals (primarily magnetite and maghemite) may be associated with senile plaques and tau filaments found in brain tissue affected by these diseases...
  56. ncbi Insulin-degrading enzyme in the Alzheimer's disease brain: prominent localization in neurons and senile plaques
    H G Bernstein
    Department of Psychiatry, University of Magdeburg, Germany
    Neurosci Lett 263:161-4. 1999
    ..In AD brains immunostaining appeared stronger than in controls and appeared not only in neurons but also in senile plaques. In a probable case of Lewy body variant of AD Lewy bodies in neurons of the Nuc...
  57. pmc Abeta42 is essential for parenchymal and vascular amyloid deposition in mice
    Eileen McGowan
    Department Neuroscience, Mayo Clinic College of Medicine, Jacksonville, FL 32224, USA
    Neuron 47:191-9. 2005
    ..These data establish that Abeta1-42 is essential for amyloid deposition in the parenchyma and also in vessels...
  58. ncbi Noradrenaline deficiency in brain increases beta-amyloid plaque burden in an animal model of Alzheimer's disease
    Sergey Kalinin
    Department of Anesthesiology, University of Illinois, and Jesse Brown Veteran s Affairs Research Division, Chicago, IL 60612, United States
    Neurobiol Aging 28:1206-14. 2007
    ..These findings suggest that noradrenergic innervation from LC are needed to maintain adequate Abeta clearance, and therefore that LC degeneration could contribute to AD pathogenesis...
  59. ncbi Three-dimensional structures of canine senile plaques
    K Miyawaki
    Department of Veterinary Pathology, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Japan
    Acta Neuropathol 102:321-8. 2001
    In this study, the three-dimensional structures of two types of canine senile plaques (SP), diffuse plaques (DP) and mature plaques (MP), were compared using a confocal laser scanning microscope...
  60. ncbi Effect of statins on beta-amyloid metabolism in humans: potential importance for the development of senile plaques in Alzheimer's disease
    K Hoglund
    Section of Experimental Neurochemistry, Institute of Clinical Neuroscience, Goteborg University, Sweden
    Acta Neurol Scand Suppl 185:87-92. 2006
    ..The pleiotropic effects of statins should be investigated further. One approach is presented in this review...
  61. ncbi Senile plaques do not induce susceptibility effects in T2*-weighted MR microscopic images
    Marc Dhenain
    Curie Institute, U350 INSERM, Centre Universitaire Laboratoire 112, 91405 Orsay Cedex, France
    NMR Biomed 15:197-203. 2002
    b>Senile plaques are the hallmarks of Alzheimer's disease. They typically range from 16 to 150 microm in size with most less than 25 microm...
  62. ncbi Amyloid plaques and amyloid-beta oligomers: an ongoing debate
    Sylvain Lesne
    Department of Neurology, University of Minnesota, Minneapolis, Minnesota 55455, USA
    J Neurosci 25:9319-20. 2005
  63. ncbi Plaques, tangles, and memory loss in mouse models of neurodegeneration
    Jason L Eriksen
    Department of Neuroscience, Mayo Clinic Jacksonville, 4500 San Pablo Road, Jacksonville, FL 32224, USA
    Behav Genet 37:79-100. 2007
    ..In this review, we discuss the status of transgenic mouse models and review the complex relationship between pathology and behavior in the development of neuropathological syndromes in AD...
  64. pmc Apolipoprotein E isoform-dependent amyloid deposition and neuritic degeneration in a mouse model of Alzheimer's disease
    D M Holtzman
    Department of Neurology, Center for the Study of Nervous System Injury, Washington University School of Medicine, 660 South Euclid Avenue, Box 8111, St Louis, MO 63110, USA
    Proc Natl Acad Sci U S A 97:2892-7. 2000
    ..Our data demonstrate a critical and isoform-specific role for apoE in neuritic plaque formation, a pathological hallmark of AD...
  65. ncbi Amyloid cored plaques in Tg2576 transgenic mice are characterized by giant plaques, slightly activated microglia, and the lack of paired helical filament-typed, dystrophic neurites
    Atsushi Sasaki
    Department of Pathology, Gunma University School of Medicine, 3 39 22 Showa machi, Maebashi, Gunma 371 8511, Japan
    Virchows Arch 441:358-67. 2002
    ....
  66. pmc Amyloid-beta vaccination, but not nitro-nonsteroidal anti-inflammatory drug treatment, increases vascular amyloid and microhemorrhage while both reduce parenchymal amyloid
    D M Wilcock
    Department of Molecular Pharmacology and Physiology, School of Basic Biomedical Science, College of Medicine, University of South Florida, 12901 Bruce B Downs Boulevard, MDC Box 9, Tampa, FL 33612, USA
    Neuroscience 144:950-60. 2007
    ..The difference between these treatments with respect to vascular amyloid development may reflect the clearance-promoting actions of the vaccine as opposed to the production-modifying effects proposed for flurbiprofen...
  67. ncbi Amyloid deposition precedes tangle formation in a triple transgenic model of Alzheimer's disease
    Salvatore Oddo
    Department of Neurobiology and Behavior, University of California, 1109 Gillespie Neuroscience Research Facility, Irvine, CA 92697 4545, USA
    Neurobiol Aging 24:1063-70. 2003
    ....
  68. ncbi Locus ceruleus degeneration promotes Alzheimer pathogenesis in amyloid precursor protein 23 transgenic mice
    Michael T Heneka
    Department of Neurology, University of Bonn, 53127 Bonn, Germany
    J Neurosci 26:1343-54. 2006
    ..Our data demonstrate that the degeneration of LC affects morphology, metabolism, and function of amyloid plaque-containing higher brain regions in APP23 mice. We postulate that LC degeneration substantially contributes to AD development...
  69. pmc Contribution by synaptic zinc to the gender-disparate plaque formation in human Swedish mutant APP transgenic mice
    Joo Yong Lee
    National Creative Research Initiative Center for the Study of Central Nervous System Zinc and Department of Neurology, University of Ulsan College of Medicine, Seoul 138 736, Korea
    Proc Natl Acad Sci U S A 99:7705-10. 2002
    ..Hence, of endogenous metals, synaptic zinc contributes predominantly to amyloid deposition in hAPP(+) mice...
  70. ncbi Mice deficient in BACE1, the Alzheimer's beta-secretase, have normal phenotype and abolished beta-amyloid generation
    Y Luo
    Amgen, One Amgen Center Drive, MS 29 2 B, Thousand Oaks, California 91320, USA
    Nat Neurosci 4:231-2. 2001
  71. ncbi 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
    In Alzheimer's disease, amyloid-beta peptide aggregates in the extracellular space to form senile plaques. The process of plaque deposition and growth has been modeled on the basis of in vitro experiments in ways that lead to divergent ..
  72. ncbi Human apolipoprotein E4 alters the amyloid-beta 40:42 ratio and promotes the formation of cerebral amyloid angiopathy in an amyloid precursor protein transgenic model
    John D Fryer
    Department of Neurology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Neurosci 25:2803-10. 2005
    ....
  73. ncbi Endogenous brain cytokine mRNA and inflammatory responses to lipopolysaccharide are elevated in the Tg2576 transgenic mouse model of Alzheimer's disease
    L M Sly
    Pharmacology, Pharmacia Corp, Kalamazoo, MI 49007, USA
    Brain Res Bull 56:581-8. 2001
    ..We demonstrate that Abeta plaques elicit inflammatory responses in Tg2576 mice that are further exacerbated when challenged by an exogenous inflammatory insult, which may serve to amplify degenerative processes...
  74. ncbi Increased plaque burden in brains of APP mutant MnSOD heterozygous knockout mice
    Feng Li
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University, 525 East 68th Street, New York, NY 10021, USA
    J Neurochem 89:1308-12. 2004
    ..These results indicate that oxidative stress can promote the pathogenesis of AD and further support the feasibility of antioxidant approaches for AD therapy...
  75. ncbi Complement association with neurons and beta-amyloid deposition in the brains of aged individuals with Down Syndrome
    E Head
    Institute for Brain Aging and Dementia, University of California, Irvine, California 92697-4540, USA
    Neurobiol Dis 8:252-65. 2001
    ..C1q-positive neurons were associated with activated microglia. These results provide evidence for Abeta-mediated inflammatory factors contributing to the rapid accumulation of neuropathology in DS brain...
  76. ncbi Intracellular mechanisms of amyloid accumulation and pathogenesis in Alzheimer's disease
    C Glabe
    Department of Molecular Biology and Biochemistry, University of California, Irvine 92697, USA
    J Mol Neurosci 17:137-45. 2001
    ..be further digested to the protease-resistant A(beta)n-42 core, perhaps by microglia, where it accumulates as senile plaques. Thus, the dystrophic neurites are likely to be the source of the immediate precursors of amyloid in the ..
  77. ncbi Enhanced neurofibrillary degeneration in transgenic mice expressing mutant tau and APP
    J Lewis
    Birdsall Building, Mayo Clinic Jacksonville, 4500 San Pablo Road, Jacksonville, FL 32224, USA
    Science 293:1487-91. 2001
    ..The interaction between Abeta and tau pathologies in these mice supports the hypothesis that a similar interaction occurs in Alzheimer's disease...
  78. ncbi Time sequence of maturation of dystrophic neurites associated with Abeta deposits in APP/PS1 transgenic mice
    Veronique Blanchard
    Neurodegenerative Disease Group, Centre de Recherche de Paris, Aventis Pharma 94403, Vitry sur Seine Cedex, France
    Exp Neurol 184:247-63. 2003
    ..The present study demonstrates that oxidative and mitochondrial stress factors are present at several phases of Abeta pathology progression, confirming the neuronal dysfunction in APP transgenic mice...
  79. pmc Hippocampal neuron loss exceeds amyloid plaque load in a transgenic mouse model of Alzheimer's disease
    Christoph Schmitz
    Department of Psychiatry and Neuropsychology, Division of Cellular Neuroscience, University of Maastricht, Maastricht, The Netherlands
    Am J Pathol 164:1495-502. 2004
    ..These findings point to the potential involvement of more than one mechanism in hippocampal neuron loss in this APP/PS-1 double-transgenic mouse model of Alzheimer's disease...
  80. pmc Effects of prolonged angiotensin-converting enzyme inhibitor treatment on amyloid beta-protein metabolism in mouse models of Alzheimer disease
    Matthew L Hemming
    Center for Neurologic Diseases, Brigham and Women s Hospital and Harvard Medical School, Boston, MA 02115, USA
    Neurobiol Dis 26:273-81. 2007
    ..Furthermore, we find no change in plaque deposition or in peripheral Abeta levels. Data from these Alzheimer models suggest that captopril and similar ACE inhibitors do not cause Abeta accumulation in vivo...
  81. pmc Dense-core senile plaques in the Flemish variant of Alzheimer's disease are vasocentric
    Samir Kumar-Singh
    Department of Molecular Genetics, University of Antwerp, Antwerp, Belgium
    Am J Pathol 161:507-20. 2002
    Alzheimer's disease (AD) is characterized by deposition of beta-amyloid (Abeta) in diffuse and senile plaques, and variably in vessels...
  82. ncbi Correlation between Abetax-40-, Abetax-42-, and Abetax-43-containing amyloid plaques and cognitive decline
    S Parvathy
    Laboratory of Molecular Neuropsychiatry, Mount Sinai School of Medicine, One Gustave L. Levy Place, Box 1230, New York, NY 10029, USA
    Arch Neurol 58:2025-32. 2001
    CONTEXT: Accumulation of senile plaques containing amyloid beta (Abeta)-protein is a pathologic hallmark of Alzheimer disease...
  83. ncbi Immunohistochemistry for the prion protein: comparison of different monoclonal antibodies in human prion disease subtypes
    Gabor G Kovacs
    Institute of Neurology, University of Vienna, and Austrian Reference Centre for Human Prion Diseases
    Brain Pathol 12:1-11. 2002
    ..of certain neurons in all cases irrespective of disease, and staining at the periphery and/or throughout the senile plaques of AD patients were also noted...
  84. ncbi Aging-related down-regulation of neprilysin, a putative beta-amyloid-degrading enzyme, in transgenic Tg2576 Alzheimer-like mouse brain is accompanied by an astroglial upregulation in the vicinity of beta-amyloid plaques
    Jenny Apelt
    Paul Flechsig Institute for Brain Research, Department of Neurochemistry, University of Leipzig, Jahnallee 59, D 04109 Leipzig, Germany
    Neurosci Lett 339:183-6. 2003
    ....
  85. ncbi Plaque-associated disruption of CSF and plasma amyloid-beta (Abeta) equilibrium in a mouse model of Alzheimer's disease
    Ronald B DeMattos
    Center for the Study of Nervous System Injury, Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Neurochem 81:229-36. 2002
    ..These findings suggest that there is a dynamic equilibrium between CNS and plasma Abeta, and that plaques create a new equilibrium because soluble CNS Abeta not only enters the plasma but also deposits onto amyloid plaques in the CNS...
  86. pmc Mostly separate distributions of CLAC- versus Abeta40- or thioflavin S-reactivities in senile plaques reveal two distinct subpopulations of beta-amyloid deposits
    Hisatomo Kowa
    Department of Neuropathology and Neuroscience, Graduate School of Pharmaceutical Sciences, University of Tokyo, 7 3 1 Bunkyo ku, Hongo, Tokyo 113 0033, Japan
    Am J Pathol 165:273-81. 2004
    Collagenous Alzheimer amyloid plaque component (CLAC) is a unique non-Abeta amyloid component of senile plaques (SP) derived from a transmembrane collagen termed CLAC-precursor...
  87. ncbi Chemotactic signaling, microglia, and Alzheimer's disease senile plaques: is there a connection?
    Magdalena Luca
    Massachusetts College of Pharmacy and Health Sciences, School of Arts and Sciences, 179 Longwood Avenue, Boston, MA 021 15 5896, USA
    Bull Math Biol 65:693-730. 2003
    ..that lead to aggregation of microglia and formation of local accumulations of chemicals observed in AD senile plaques. We develop a model for chemotaxis in response to a combination of chemoattractant and chemorepellent ..
  88. ncbi A Phase II study targeting amyloid-beta with 3APS in mild-to-moderate Alzheimer disease
    P S Aisen
    Department of Neurology, Georgetown University Medical Center, Washington, DC, USA
    Neurology 67:1757-63. 2006
    ....
  89. pmc Vaccination of Alzheimer's model mice with Abeta derivative in alum adjuvant reduces Abeta burden without microhemorrhages
    Ayodeji A Asuni
    Department of Psychiatry, New York University School of Medicine, Millhauser Laboratories, 560 First Avenue, New York, NY 10016, USA
    Eur J Neurosci 24:2530-42. 2006
    ..These findings indicate that our approach age-dependently improves cognition and reduces Abeta burden when used with an adjuvant suitable for humans, without increasing vascular Abeta deposits or microhemorrhages...
  90. ncbi 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
    Postmortem analyses of senile plaques reveal numerous dystrophic processes in their vicinity...
  91. ncbi The use of formic acid to embellish amyloid plaque detection in Alzheimer's disease tissues misguides key observations
    Michael R D'Andrea
    Johnson and Johnson Pharmaceutical Research and Development, Drug Discovery, Welsh and McKean Roads, Spring House, PA 19477 0776, USA
    Neurosci Lett 342:114-8. 2003
    ..The obvious benefits of formic acid for increasing the sensitivity of amyloid plaque immunolabeling may artifactually emphasize plaques over amyloid-containing cells during analyses...
  92. pmc Loss of neprilysin function promotes amyloid plaque formation and causes cerebral amyloid angiopathy
    Wesley Farris
    Center for Neurologic Diseases, Department of Neurology, Harvard Institutes of Medicine, Room 730, Boston, MA 02115, USA
    Am J Pathol 171:241-51. 2007
    ....
  93. ncbi In-vivo imaging of Alzheimer disease beta-amyloid with [11C]SB-13 PET
    Nicolaas P L G Verhoeff
    Vivian Rakoff PET Centre, Centre for Addiction and Mental Health, Ontario, Canada
    Am J Geriatr Psychiatry 12:584-95. 2004
    ..The authors' aim was to develop a novel Abeta-specific positron-emission tomography (PET) tracer...
  94. ncbi Neprilysin gene transfer reduces human amyloid pathology in transgenic mice
    Robert A Marr
    Laboratory of Genetics, The Salk Institute for Biological Studies, La Jolla, California 92037, USA
    J Neurosci 23:1992-6. 2003
    ..These data further support a role for neprilysin in regulating cerebral amyloid deposition and suggest that gene transfer approaches might have potential for the development of alternative therapies for Alzheimer's disease...
  95. ncbi Efficacy of anti-Abeta antibody isotypes used for intracerebroventricular immunization in TgCRND8
    Neelima B Chauhan
    Research and Development 151, Jesse Brown VA Medical Center Chicago, 820 South Damen Avenue, Chicago, IL 60612, USA
    Neurosci Lett 375:143-7. 2005
    ..Intriguingly, there was no significant difference between the Abeta-reducing efficiency of IgG1 anti-Abeta antibodies directed against residues 3-6, against residues 1-10 or against residues 1-28 of N-terminus Abeta...
  96. ncbi The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics
    John Hardy
    Laboratories of Neurogenetics, National Institute on Aging, Bethesda, MD 20892, USA
    Science 297:353-6. 2002
    ..The rest of the disease process, including formation of neurofibrillary tangles containing tau protein, is proposed to result from an imbalance between Abeta production and Abeta clearance...
  97. ncbi A century of Alzheimer's disease
    Michel Goedert
    Laboratory of Molecular Biology, Medical Research Council, Cambridge CB2 2QH, UK
    Science 314:777-81. 2006
    ..Genetic studies have shown that dysfunction of amyloid-beta or tau is sufficient to cause dementia. The ongoing molecular dissection of the neurodegenerative pathways is expected to lead to a true understanding of disease pathogenesis...
  98. ncbi Deglycosylated anti-amyloid-beta antibodies eliminate cognitive deficits and reduce parenchymal amyloid with minimal vascular consequences in aged amyloid precursor protein transgenic mice
    Donna M Wilcock
    Department of Pharmacology and Molecular Therapeutics, University of South Florida, Tampa, Florida 33612, USA
    J Neurosci 26:5340-6. 2006
    ....
  99. ncbi Collagen XVIII: a novel heparan sulfate proteoglycan associated with vascular amyloid depositions and senile plaques in Alzheimer's disease brains
    Jack van Horssen
    Department of Pathology, University Medical Center, Nijmegen, The Netherlands
    Brain Pathol 12:456-62. 2002
    Heparan sulfate proteoglycans (HSPGs) may play a role in the formation and persistence of senile plaques and neurofibrillary tangles in Alzheimer's disease brains...
  100. ncbi Diffuse plaques associated with astroglial amyloid beta protein, possibly showing a disappearing stage of senile plaques
    H Yamaguchi
    Gunma University School of Health Sciences, Japan
    Acta Neuropathol 95:217-22. 1998
    To clarify whether senile plaques disappear, we examined amyloid beta protein (A beta) deposits in non-demented subjects, and found novel diffuse plaques associated with astroglial A beta...
  101. ncbi Selective PrP-like protein, doppel immunoreactivity in dystrophic neurites of senile plaques in Alzheimer's disease
    I Ferrer
    Institut de Neuropatologia, Servei Anatomia Patològica, Hospital de Bellvitge, Universitat de Barcelona, Hospitalet de Llobregat, Spain
    Neuropathol Appl Neurobiol 30:329-37. 2004
    ..No modifications in Dpl immunoreactivity were observed in CJD excepting those associated with accompanying senile plaques. No Dpl-positive deposits were seen in FFI...

Research Grants64

  1. Statin modulation of immunotherapy for Alzheimer disease
    Jun Tan; Fiscal Year: 2012
    ..It is pathologically characterized by the presence of extracellular senile plaques in the brain primarily composed of 40-42 amino acid length amyloid beta (A(1-40, 42) peptides...
  2. Zhongcong Xie; Fiscal Year: 2016
    ..unreadable]-Amyloid protein (A[unreadable]) is th key component of senile plaques in Alzheimer's disease (AD) patients, and A[unreadable] levels are elevated in the brains of AD patients ..
  3. Glucose Metabolic, Amyloid, and Tau Brain Imaging in Down's Syndrome and Dementia
    GARY WILLIAM SMALL; Fiscal Year: 2013
    ..Down's syndrome (DS) exhibit the neuropathological hallmarks of Alzheimer's disease (AD): amyloid senile plaques (SPs) and tau neurofibrillary tangles (NFTs)...
  4. Extracellular Zinc Buffering and A-beta Oligomerization
    GUIDO FAAS; Fiscal Year: 2012
    ..proteopathy leading to intracellular accumulation of tau protein and extracellular amyloid 2 (Ab) aggregates (senile plaques)...
  5. Bernard G Schreurs; Fiscal Year: 2015
    ..appears to be elevated in the blood of Alzheimer's patients, and is one of the trace metals found in senile plaques of post-mortem Alzheimer's brains...
  6. Andrea Joan Tenner; Fiscal Year: 2014
    ..changes seen in AD brain include synaptic and neuronal loss, neurofibrillary tangles (NFTs), extracellular senile plaques composed of amyloid (A[unreadable]) protein deposits and evidence of inflammatory events...
  7. Huaxi Xu; Fiscal Year: 2016
    ..disease (AD) is overproduction/accumulation of ?-amyloid (A?) peptides that form extracellular senile plaques in the brain...
  8. Beta-Amyloid Immunization in a Canine Model of Aging
    Elizabeth Head; Fiscal Year: 2013
    Alzheimer's disease (AD) is associated with progressive cognitive decline and the accumulation of senile plaques and neurofibrillary tangles...
  9. AMYLOID PLAQUE AND TANGLE IMAGING IN AGING AND DEMENTIA
    GARY WILLIAM SMALL; Fiscal Year: 2010
    Amyloid senile plaques (SPs) and neurofibrillary tangles (NFTs) are neuropathological hallmarks of Alzheimer's disease (AD) that also accumulate in key brain regions in association with normal aging...
  10. Cyclohexanehexol Therapy in Transgenic Models of Alzheimer's Disease
    Alpaslan Dedeoglu; Fiscal Year: 2013
    Project Summary/Abstract Senile plaques that contain beta amyloid (Ass) and neurofibrillary tangles (NFT) with phosphorylated tau are the pathological hallmarks of Alzheimer's disease (AD)...
  11. ROLE OF HSP 110 IN TAUOPATHY
    Nahid F Mivechi; Fiscal Year: 2013
    ..The neuropathological hallmarks of AD and other tauopathies include accumulation of senile plaques and/or neurofibrillary tangles (NFTs) that causes neurons to degenerate...
  12. Post-translational Modifications of Proteins in Parkinson?s disease
    Jing Zhang; Fiscal Year: 2012
    ..formation of Lewy bodies (LBs) or Alzheimer's changes (presence of neurofibrillary tangles (NfTs) and senile plaques (SPs)) in the cortex...
  13. Mucosal Immunotherapy in a mouse model of Alzheimer's Disease
    Howard L Weiner; Fiscal Year: 2010
    ..for Abeta in the regions lacking Abeta deposits and investigators have reported a local reduction of senile plaques in a neocortical region affected by incomplete ischemia in a case of AD with stroke...
  14. CutA interacts with BACE1 and participates in Alzheimer's disease
    Yunwu Zhang; Fiscal Year: 2012
    DESCRIPTION (provided by applicant): An important pathologic feature of AD is the formation of extracellular senile plaques in the brain, whose major component is a small peptide called ?-amyloid (A?)...
  15. Effect of RanbpM on amyloid pathology in a mouse model of Alzheimer's disease
    MADEPALLI KRISHNAPPA LAKSHMANA; Fiscal Year: 2009
    ..provided by applicant): The pathological hallmarks of Alzheimer's disease (AD) are the presence of senile plaques, largely composed of extracellular deposits of amyloid beta (A2) peptide and intracellular neurofibrillary ..
  16. Regulatory RNAs as mediators and biomarkers in Alzheimer's Disease
    CLAES ROBERT WAHLESTEDT; Fiscal Year: 2012
    ..link between amyloid pathway and AD and in the precedence of events leading to AD, deposition of A2 1-42 into senile plaques is a proven feature of AD neuropathology...
  17. Yoshitaka Ishii; Fiscal Year: 2014
    ..The formation of senile plaques in a brain is a hall mark of Alzheimer's disease (AD);the primary component of the plaque is fibrillar ..
  18. Molecular Motors in Transport and Signaling by APP
    Virgil Muresan; Fiscal Year: 2009
    ..of amyloid precursor protein (APP), the precursor of amyloid beta peptide, which forms the extracellular senile plaques in Alzheimer's disease...
  19. Riqiang Yan; Fiscal Year: 2016
    ..abstract_text> ..
  20. Bradley T Hyman; Fiscal Year: 2015
    ..neurons cultured from Tg2576 (APPSw) mice develop the same sort of neurodegenerative phenotype that occur near senile plaques in the adult Tg mouse or human Alzheimer brain - loss of dendritic spines, simplification of dendritic ..
  21. Apolipoprotein E receptors and Alzheimers disease
    G William Rebeck; Fiscal Year: 2010
    ..is induced acutely after several types of brain damage, and is present in AD chronically as a component of senile plaques. We will examine how apoE affects processes in vivo using three systems: injection of apoE into the brain ..
  22. Small vessel disease and beta-amyloid deposition in mildly impaired cognition
    Eric E Smith; Fiscal Year: 2012
    ..pathological brain changes associated with Alzheimer's disease (including neurofibrillary tangles and senile plaques) modify the relationship between small vessel disease and cognition, there is a critical need to incorporate ..
  23. The neurogenic potential of cholinergic activation in AD.
    ELIZABETH ADAMS ECKMAN; Fiscal Year: 2013
    ..characterized by three major pathological findings, the abnormal accumulation of A[unreadable] in the form of senile plaques, the presence of neurofibrillary tangles (NFTs) and the existence of substantial cell loss and dysfunction in ..
  24. Robert K Yu; Fiscal Year: 2015
    ..Since gangliosides are expressed in senile plaques in AD and appear to interact with A2s and APP, they can potentially be exploited as therapeutic agents for the ..
  25. Novel PET Ligands for In Vivo Binding to Amyloid in AD
    Brian J Ciliax; Fiscal Year: 2010
    ..The two hallmark defects of AD are senile plaques (SP) and neurofibrillary tangles (NFT)...
  26. Toll-Like Receptor Signaling in Alzheimer's Disease
    Kathryn J Moore; Fiscal Year: 2013
    ..disease (AD) these cells bind B-amyloid (AB) and accumulate at sites of AB deposition, including senile plaques. Microglial interactions with AB promote a chronic inflammatory response characterized by the production of ..
  27. Zhongcong Xie; Fiscal Year: 2016
    ..activation and apoptosis, which in turn increases generation of amyloid 2-protein (A2), the key component of senile plaques in AD patients...
  28. Miroslav Peric; Fiscal Year: 2015
    ..disease is characterized pathologically by abnormal depositions of ? amyloid proteins in the brain, called senile plaques. Unfortunately, the pathophysiological role of the ?-amyloid peptides in causing Alzheimer's disease and ..
  29. Structural Facets of the Inhibition of Alzheimer's Amyloid-beta Oligomers by Tric
    Nathan A Oyler; Fiscal Year: 2012
    ..it is widely believed that the A[unreadable] protein, the major component of the observed extracellular senile plaques (amyloid fibrils) in the brains of Alzheimer's patients, is intimately and causally related to the ..
  30. Cognitive Effects of Intracellular Targeted and FAD-linked Mutant Amyloid Betas
    CHRISTOPHER GEORGE JANUS; Fiscal Year: 2012
    DESCRIPTION (provided by applicant): The accumulation of amyloid [unreadable] peptide (A[unreadable]) within senile plaques and the walls of cerebral blood vessels, as well as diffuse A[unreadable] deposits is a hallmark of Alzheimer&..
  31. Victor A Cazares; Fiscal Year: 2014
    ..Munc13 mediated vesicle priming has been shown to regulate the amyloid precursor protein which gives rise to senile plaques composed of 2-amyloid peptides characteristic of neural tissue in Alzheimer's disease patients...
  32. Age related Cognitive Loss in Mumbai, India
    Dushyant P Purohit; Fiscal Year: 2010
    ..CDR=0) for the extent and distribution of neurofibrillary tangles and beta- amyloid deposits in the form of senile plaques, diffuse plaques and vascular amyloid accumulations...
  33. Philippe Marambaud; Fiscal Year: 2016
    ..is a progressive neurodegenerative disorder characterized by A[unreadable] peptide deposition into cerebral senile plaques. CALHM1 is a recently identified neuronal calcium channel controlling AD age-at-onset and A[unreadable] levels ..
  34. Kurt R Brunden; Fiscal Year: 2014
    ..The successful completion of these studies will result in one or more novel drug candidates from a new class of AD therapeutics that will have the potential of decreasing A peptides and senile plaques in the AD brain.
  35. Mechanisms Underlying the Vascular Pathology of Alzheimer's Disease
    Gregory A Elder; Fiscal Year: 2012
    ..Although less studied than senile plaques and neurofibrillary tangles, AD is also accompanied by microvascular pathology...
  36. Synaptic damage in models of beta-amyloid associated pathology
    Edward H Koo; Fiscal Year: 2011
    ..Amyloid beta-protein, the major constituent of senile plaques in brain, has been shown to impair synaptic function both in vitro and in vivo...
  37. Reporter Mice For APP Processing And Transport
    Zoia Muresan; Fiscal Year: 2012
    ..APP, the precursor of the amyloid-? peptide that forms the senile plaques in AD, is proteolytically cleaved, by the action of secretases, into soluble, N-terminal (sAPP) and C-terminal ..
  38. Xinglong Wang; Fiscal Year: 2014
    ..disease (AD) is the leading cause of dementia in the elderly, characterized by neurofibrillary tangles, senile plaques and a progressive loss of neuronal cells in selective brain regions...
  39. AGING AND ALZHEIMER DEMENTIA--ROLE OF FIBROUS PROTEINS
    Shu Hui Yen; Fiscal Year: 2000
    ..and cell processes, in the form of neurofibrillary tangles (NFT), neuropil threads and dystrophic neurites in senile plaques. Paired helical filaments and biochemically similar 15-18 nm diameter straight filaments are composed of ..
  40. Novel Tau-mediated Neurodegeneration Mechanisms
    ADRIANA B FERREIRA; Fiscal Year: 2010
    ..during the first funded period of this project (2000-2004) led to the first evidence of a direct link between senile plaques and tau pathology in an Alzheimer's disease (AD) cell model system (Rapoport et al., 2002)...
  41. Mechanisms of Microglial Activation and Phagocytosis in*
    Gary Landreth; Fiscal Year: 2005
    ..of fibrillar forms of beta-amyloid (AB) peptides into the extracellular space, and their compaction into senile plaques. The deposition of AB is also observed in a number of animal models that overexpress the human APP gene...
  42. GLIAL B-AMYLOID PEPTIDE RECEPTORS IN ALZHEIMER'S DISEASE
    Kurt Brunden; Fiscal Year: 1993
    ..from applicant's abstract): One of the pathological hallmarks of Alzheimer's Disease is the presence of senile plaques containing beta-amyloid peptide (BAP)...
  43. MULTIFOCAL NEURODEGENERATION IN ALZHEIMER'S DISEASE
    Brent Vogt; Fiscal Year: 2002
    ..to terminate in a final common neuropathology with loss of large pyramids, neurofibrillary tangles, and senile plaques. Although well-documented clinical heterogeneity could result from random expression of a single mechanism of ..
  44. Role of Anesthetic Isoflurane in Alzheimer's Disease: In Vivo Investigation
    Zhongcong Xie; Fiscal Year: 2009
    ..inhalant anesthetic isoflurane induces caspase activation and increases generation of Ab, the key component of senile plaques in Alzheimer's disease (AD) patients...
  45. DETECTION OF EARLY DEMENTIA IN ADULTS WITH DOWN SYNDROME
    KAREN BRUGGE; Fiscal Year: 1999
    ..Although post-mortem neuropathological studies reveal senile plaques and neurofibrillary tangles in almost all DS adults over the age of 40 years...
  46. Chemokines, Microglia and Alzheimer's Disease
    Andrew Luster; Fiscal Year: 2007
    ..We propose to determine the molecular mechanism of recruitment, activation and retention of microglia in senile plaques in AD...
  47. MUSCARINIC RECEPTORS/G-PROTEINS IN EARLY AD
    Pamela Potter; Fiscal Year: 1999
    ..observed in pre-clinical stages of Alzheimer's disease, and how do these correlate with cholinergic indiced, senile plaques and levels of beta-amyloid? These experiments will be performed in samples of human brain from non- demented ..
  48. NEUROFILAMENT KINASES AND ALZHEIMERS DISEASE TAU
    RONALD LIEM; Fiscal Year: 1999
    The two major pathological hallmarks of Alzheimer's disease are the neurofibrillary tangles and the senile plaques. Senile plaques consist of extracellular amyloid fibrils, composed of the beta-amyloid peptide, a proteolytic fragment of ..
  49. CLINICAL METABOLIC CORRELATION IN DEMENTIA BY PROTON NMR
    William Klunk; Fiscal Year: 1999
    ..Much like senile plaques and neurofibrillary tangles, NAA can be considered a new candidate marker of the neuropathological severity of ..
  50. PATHOLOGY IN ALZHEIMER'S DISEASE
    Gerald Higgins; Fiscal Year: 1990
    ..Subsequent studies will be undertaken in human brain, to determine if a similar relationship exists between nerve growth factor receptor regulation and hippocampal pathology and gene expression in AD...
  51. SPECTROSCOPY FOR ALZHEIMER'S DISEASE DIAGNOSIS
    Michael Feld; Fiscal Year: 2001
    ..The demonstrated presence of unique biochemical markers (senile plaques containing amyloid fibrils and neurofibrillary tangles rich in phosphorylated proteins), will provide unique ..
  52. APOLIPOPROTEIN AND AD AMYLOID FORMATION
    Xuemin Xu; Fiscal Year: 2001
    ..1) genetic evidence suggesting that apoE is a risk factor for AD, 2) apoE presence in association in the senile plaques and in complex with Abeta in cerebrospinal fluid and plasma, 3) the formation of a stable complex between apoE ..
  53. SUPPRESSING PLAQUE ACTIVATION OF MICROGLIA IN ALZHEIMERS
    DANA GIULIAN; Fiscal Year: 2000
    ..work is based on the hypothesis that cytotoxic actions of activated microglia, reacting to neuritic and core senile plaques, contribute to the neuronal injury associated with Alzheimer's disease (AD)...
  54. Assay Development for Drugs to Reduce Neuroinflammation
    CASEY MORROW; Fiscal Year: 2004
    ..protein (MCP-1) that causes the recruitment of new microglia J monocytes to the site of lesions in MS and senile plaques in AD...
  55. NEUROTROPHIN REGULATION OF LRP IN CNS NEURONS
    Guojun Bu; Fiscal Year: 2001
    ..In addition to its role in the catabolism of its ligands, LRP itself has been identified as a component of senile plaques, a pathological hallmark of AD...
  56. Berislav V Zlokovic; Fiscal Year: 2016
    ..Apolipoproteins J and E (apoJ, apoE) co-localize with the senile plaques and congophilic angiopathy of AD...
  57. CHOLINERGIC DEFICIENCY
    Donald Schmechel; Fiscal Year: 1991
    ..Visible damage to cholinergic axons is accompanied in these animals by neuritic and senile plaques, amyloid deposits, and abnormal iron storage in peripheral organs and brain...
  58. CYTOSKELETAL DISORGANIZATION ALZHEIMER'S DISEASE
    Ann McKee; Fiscal Year: 1993
    ..and mortality in the elderly, is defined by histopathological features, notably neurofibrillary tangles and senile plaques. Because no animal model exists for the disorder, advances in understanding the pathogenesis of Alzheimer's ..
  59. High throughput tau oligomer assay for drug screening for Alzheimer's disease
    James Moe; Fiscal Year: 2007
    ..with neurofibrillary tangles (NFTs), or [unreadable]-amyloid (A-[unreadable]) protein associated with senile plaques. An in vitro system was assembled, in which key events of the tau protein misfolding and oligomerization were ..
  60. Beta-Amyloid Aggregation and Toxicity:
    REGINA MURPHY; Fiscal Year: 2003
    ..Extracellular senile plaques, one of the defining pathological features of the disease, consist of a proteinaceous amyloid deposit ..
  61. INTERACTIONS BETWEEN MICROGLIA AND BETA AMYLOID PLAQUES
    FREDERICK MAXFIELD; Fiscal Year: 2004
    DESCRIPTION (Abstract): Microglia are immune-system cells associated with senile plaques containing B-amyloid (AB) in Alzheimer's disease (AD)...
  62. Neonatal exposure & neurodegeneration of the aged brain
    Nasser Zawia; Fiscal Year: 2006
    DESCRIPTION (provided by applicant): The brains of Alzheimer's disease (AD) patients are replete with senile plaques composed mainly of the beta-amyloid (Abeta) peptide...