neurofibrils

Summary

Summary: The delicate interlacing threads, formed by aggregations of neurofilaments and neurotubules, coursing through the cytoplasm of the body of a neuron and extending from one dendrite into another or into the axon.

Top Publications

  1. ncbi The precursor of Alzheimer's disease amyloid A4 protein resembles a cell-surface receptor
    J Kang
    Nature 325:733-6. 1987
  2. ncbi Drugs targeting Alzheimer's disease: some things old and some things new
    Mary L Michaelis
    Department of Pharmacology and Toxicology, University of Kansas, Lawrence, Kansas 66045 7582, USA
    J Pharmacol Exp Ther 304:897-904. 2003
  3. ncbi Amyloid beta: the alternate hypothesis
    Hyoung-Gon Lee
    Institute of Pathology, Case Western Reserve University, Cleveland, Ohio, USA
    Curr Alzheimer Res 3:75-80. 2006
  4. ncbi Neurofibrillary pathology leads to synaptic loss and not the other way around in Alzheimer disease
    Khalid Iqbal
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, NY 10314-6399, USA
    J Alzheimers Dis 4:235-8. 2002
  5. ncbi Astrocytosis, microgliosis, metallothionein-I-II and amyloid expression in high cholesterol-fed rabbits
    Paolo Zatta
    CNR Center on Metalloproteins, Department of Biology, University of Padova, Italy
    J Alzheimers Dis 4:1-9. 2002
  6. ncbi Characterization of neuronal dystrophy induced by fibrillar amyloid beta: implications for Alzheimer's disease
    E A Grace
    Department of Neuroscience, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, CT 06030, USA
    Neuroscience 114:265-73. 2002
  7. ncbi Imaging real-time aggregation of amyloid beta protein (1-42) by atomic force microscopy
    Ashok Parbhu
    Neuroscience Research Institute, University of California, Santa Barbara, CA 93016, USA
    Peptides 23:1265-70. 2002
  8. ncbi Laminin affects polymerization, depolymerization and neurotoxicity of Abeta peptide
    Carlos Morgan
    Departamento de Biologia Celular y Molecular, MIFAB, Facultad de Ciencias Biologicas, Centro de Regulación Celular y Patología, Pontificia Universidad Catolica de Chile, Casilla 114 D, Santiago, Chile
    Peptides 23:1229-40. 2002
  9. ncbi [Advances in molecular pathology of Alzheimer's disease]
    F Coria-Balanzat
    Clínica contra las Enfermedades Nerviosas, Servicio de Neurologia, Hospital Son Dureta, Palma de Mallorca, Baleares, Spain
    Rev Neurol 42:306-9. 2006
  10. ncbi The role of cystatin C in cerebral amyloid angiopathy and stroke: cell biology and animal models
    Efrat Levy
    Department of Psychiatry, New York University School of Medicine, and Nathan Kline Institute, Orangeburg 10962, USA
    Brain Pathol 16:60-70. 2006

Research Grants

  1. The role of Mnbk in Downs Syndrome brain development and aging
    Jerzy Wegiel; Fiscal Year: 2007
  2. In Vivo Testing of Microtubule-Stabilizing Drugs in Triple Transgenic Mice
    MARY MICHAELIS; Fiscal Year: 2007
  3. Subgroups of Alzheimer Disease
    Khalid Iqbal; Fiscal Year: 2007
  4. Abnormal Hyperphosphorylation of Tau
    Khalid Iqbal; Fiscal Year: 2007
  5. Therapeutic Targeting of Abnormal Conformation in Neurodegenerative Disease
    Thomas M Wisniewski; Fiscal Year: 2010
  6. Modeling Neurofibrillary Degeneration
    Shu Hui Yen; Fiscal Year: 2007
  7. Amyloid beta Peptide and Apolipoprotein E
    Thomas Wisniewski; Fiscal Year: 2007
  8. ADDLs, synapses & the molecular etiology of Alzheimer's disease
    WILLIAM KLEIN; Fiscal Year: 2007
  9. Progression of Tau Pathology in AD
    Lester Binder; Fiscal Year: 2007
  10. Amyloid and tau pathology in a transgenic model
    Michael Hutton; Fiscal Year: 2006

Detail Information

Publications112 found, 100 shown here

  1. ncbi The precursor of Alzheimer's disease amyloid A4 protein resembles a cell-surface receptor
    J Kang
    Nature 325:733-6. 1987
    ..This sequence, together with the localization of its gene on chromosome 21, suggests that the cerebral amyloid deposited in Alzheimer's disease and aged Down's syndrome is caused by aberrant catabolism of a cell-surface receptor...
  2. ncbi Drugs targeting Alzheimer's disease: some things old and some things new
    Mary L Michaelis
    Department of Pharmacology and Toxicology, University of Kansas, Lawrence, Kansas 66045 7582, USA
    J Pharmacol Exp Ther 304:897-904. 2003
    ..Nevertheless, the pace of recent research clearly supports optimism that slowing progression of AD will soon be possible...
  3. ncbi Amyloid beta: the alternate hypothesis
    Hyoung-Gon Lee
    Institute of Pathology, Case Western Reserve University, Cleveland, Ohio, USA
    Curr Alzheimer Res 3:75-80. 2006
    ....
  4. ncbi Neurofibrillary pathology leads to synaptic loss and not the other way around in Alzheimer disease
    Khalid Iqbal
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, NY 10314-6399, USA
    J Alzheimers Dis 4:235-8. 2002
  5. ncbi Astrocytosis, microgliosis, metallothionein-I-II and amyloid expression in high cholesterol-fed rabbits
    Paolo Zatta
    CNR Center on Metalloproteins, Department of Biology, University of Padova, Italy
    J Alzheimers Dis 4:1-9. 2002
    ..The relevance on the cholesterol metabolism in Alzheimer's disease pathogenesis is also discussed...
  6. ncbi Characterization of neuronal dystrophy induced by fibrillar amyloid beta: implications for Alzheimer's disease
    E A Grace
    Department of Neuroscience, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, CT 06030, USA
    Neuroscience 114:265-73. 2002
    ..These results suggest that aberrant plastic changes and loss of synaptic integrity induced by fibrillar Abeta may play a significant role in the development of AD pathology...
  7. ncbi Imaging real-time aggregation of amyloid beta protein (1-42) by atomic force microscopy
    Ashok Parbhu
    Neuroscience Research Institute, University of California, Santa Barbara, CA 93016, USA
    Peptides 23:1265-70. 2002
    ..These results strongly suggest that no AbetaP-fibers are formed for the physiologically relevant concentration and thus the plaque-associated fibers may not account for the AD pathophysiology...
  8. ncbi Laminin affects polymerization, depolymerization and neurotoxicity of Abeta peptide
    Carlos Morgan
    Departamento de Biologia Celular y Molecular, MIFAB, Facultad de Ciencias Biologicas, Centro de Regulación Celular y Patología, Pontificia Universidad Catolica de Chile, Casilla 114 D, Santiago, Chile
    Peptides 23:1229-40. 2002
    ....
  9. ncbi [Advances in molecular pathology of Alzheimer's disease]
    F Coria-Balanzat
    Clínica contra las Enfermedades Nerviosas, Servicio de Neurologia, Hospital Son Dureta, Palma de Mallorca, Baleares, Spain
    Rev Neurol 42:306-9. 2006
    ..Alzheimer's disease (AD) results from the progressive accumulation of a specific protein (beta peptide) in the brain parenchyma in the form of amyloid deposits...
  10. ncbi The role of cystatin C in cerebral amyloid angiopathy and stroke: cell biology and animal models
    Efrat Levy
    Department of Psychiatry, New York University School of Medicine, and Nathan Kline Institute, Orangeburg 10962, USA
    Brain Pathol 16:60-70. 2006
    ..This review focuses on cell culture and animal models used to study the role of cystatin C in these processes...
  11. ncbi Region-specific dissociation of neuronal loss and neurofibrillary pathology in a mouse model of tauopathy
    Tara L Spires
    Department of Neurology, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Charlestown 02129, USA
    Am J Pathol 168:1598-607. 2006
    ..Together, these results imply that neurofibrillary tangles do not necessarily lead to neuronal death...
  12. ncbi ADDLs & protofibrils--the missing links?
    William L Klein
    Cognitive Neurology and Alzheimer s Disease Center, Northwestern University Institute for Neuroscience, Evanston, IL 60208, USA
    Neurobiol Aging 23:231-5. 2002
  13. ncbi Structure and location of amyloid beta peptide chains and arrays in Alzheimer's disease: new findings require reevaluation of the amyloid hypothesis and of tests of the hypothesis
    William I Rosenblum
    Medical College of Virginia at Virginia Commonwealth University, Richmond VA, USA
    Neurobiol Aging 23:225-30. 2002
    ....
  14. ncbi Synthesis of 6-[2-(benzoxazol-2-ylmethylamino)ethoxy]-1-alkyl-1H-indole-2-carboxylic acid and inhibitory activity on beta-amyloid aggregation
    Sun Mi Lee
    College of Pharmacy, Sookmyung Women's University, Seoul 140-742, Korea
    Arch Pharm Res 28:1219-23. 2005
    ..Their inhibitory activity on Abeta, aggregation was evaluated by thioflavin T assay although their activities were insignificant...
  15. ncbi Hippocampal apolipoprotein D level depends on Braak stage and APOE genotype
    F Glockner
    Institute of Anatomy, Department of Clinical Cell and Neurobiology, Charite, 10098 Berlin, Germany
    Neuroscience 122:103-10. 2003
    ..This increase, however, was restricted to the APOE epsilon3/3 group, whereas the APOE epsilon4 group did not show significant variations in hippocampal apoD...
  16. ncbi Effects of lipids and aging on the neurotoxicity and neuronal loss caused by intracerebral injections of the amyloid-beta peptide in the rat
    A Gonzalo-Ruiz
    Laboratory of Neuroanatomy, Institute of Neuroscience of Castilla and Leon, Valladolid University, Nicolas Rabal Street, 17, 42003 Soria, Spain
    Exp Neurol 197:41-55. 2006
    ..In conclusion, our findings indicate an interaction between lipids, age, and Abeta neurotoxicity, and might provide insights into the basic mechanisms involved in a short-term (acute-to-subchronic) response to Abeta peptide...
  17. ncbi Tau, tangles, and Alzheimer's disease
    Lester I Binder
    Department of Cell and Molecular Biology, Feinberg School of Medicine, Northwestern University, 303 E Chicago Avenue, Chicago, IL 60611, USA
    Biochim Biophys Acta 1739:216-23. 2005
    ..In this review, we discuss evidence that strongly suggests that these truncations occur in an orderly pattern and directly influence the ability of tau to polymerize into filaments...
  18. ncbi Tau pathology in Alzheimer disease and other tauopathies
    Khalid Iqbal
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, NY 10314 6399, USA
    Biochim Biophys Acta 1739:198-210. 2005
    ..Inhibition of this tau abnormality is one of the most promising therapeutic approaches to AD and other tauopathies...
  19. ncbi In vitro model of neurotoxicity of Abeta 1-42 and neuroprotection by a pentapeptide: irreversible events during the first hour
    Zsolt Datki
    Department of Medical Chemistry, University of Szeged, Szeged, Hungary
    Neurobiol Dis 17:507-15. 2004
    ..A novel pentapeptide LPYFD-amide, an analog of Soto's LPFFD, significantly decreased neurite degeneration, tau aggregation, and cell viability reduction induced by Abeta 1-42...
  20. ncbi Vitamin A exhibits potent antiamyloidogenic and fibril-destabilizing effects in vitro
    Kenjiro Ono
    Department of Neurology and Neurobiology of Aging, Kanazawa University Graduate School of Medical Science, Kanazawa 920-8640, Japan
    Exp Neurol 189:380-92. 2004
    ..Although the exact mechanisms are still unclear, vitamins A and beta-carotene could be key molecules for the prevention and therapy of AD...
  21. ncbi Calpain mediates calcium-induced activation of the erk1,2 MAPK pathway and cytoskeletal phosphorylation in neurons: relevance to Alzheimer's disease
    Takahide Kaji
    Center for Dementia Research, Nathan Kline Institute for Psychiatric Research, Orangeburg, New York, USA
    Am J Pathol 165:795-805. 2004
    ....
  22. ncbi ApoE and Abeta1-42 interactions: effects of isoform and conformation on structure and function
    Arlene M Manelli
    Department of Medicine, Division of Geriatrics, Evanston Northwestern Healthcare Research Institute, Evanston, Illinois 60201, USA
    J Mol Neurosci 23:235-46. 2004
    ..We will continue to investigate the effect of apoE isoform and Abeta conformation on the structural and functional interactions between these two proteins in relation to the pathogenesis of AD...
  23. ncbi Protein misfolding in neurodegenerative diseases
    E I Agorogiannis
    University of Thessaly Medical School, Department of Neurology and Neurogenetics, Larissa, Greece
    Neuropathol Appl Neurobiol 30:215-24. 2004
    ....
  24. ncbi [Research progress on Alzheimer's disease: pathogenesis and medical therapy]
    Shu Li Sheng
    Beijing Key Lab for Brain Aging, Xuanwu Hospital, Capital University of Medical Sciences, Beijing 100053, China
    Zhongguo Yi Xue Ke Xue Yuan Xue Bao 26:101-3. 2004
    ..In this article, we discuss the mechanisms of AD in four aspects and put forward the strategies of drug therapy...
  25. ncbi Memantine inhibits and reverses the Alzheimer type abnormal hyperphosphorylation of tau and associated neurodegeneration
    Liang Li
    Department of Neurochemistry, NYS Institute for Basic Research, 1050 Forest Hill Road, Staten Island, NY 10314-6399, USA
    FEBS Lett 566:261-9. 2004
    ....
  26. ncbi Proteolytic generation and aggregation of peptides from transmembrane regions: lung surfactant protein C and amyloid beta-peptide
    J Johansson
    Department of Molecular Biosciences, Swedish University of Agricultural Sciences, The Biomedical Centre, 751 23, Uppsala, Sweden
    Cell Mol Life Sci 61:326-35. 2004
    ..We speculate that the loss of structural context for sequences with a high propensity for formation of beta sheets may be a common feature of amyloid formation in general...
  27. ncbi Protein quality control in Alzheimer's disease: a fatal saviour
    W Scheper
    Neurogenetics Laboratory, Academic Medical Center, P O Box 22700, 1100 DE Amsterdam, The Netherlands
    Curr Drug Targets CNS Neurol Disord 4:283-92. 2005
    ..In this review, we will discuss the role of protein quality control in the neurotoxicity of Abeta...
  28. ncbi Polymerization of hyperphosphorylated tau into filaments eliminates its inhibitory activity
    Alejandra del C Alonso
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, NY 10314 6399, USA
    Proc Natl Acad Sci U S A 103:8864-9. 2006
    ....
  29. ncbi Up-regulation of mitogen-activated protein kinases ERK1/2 and MEK1/2 is associated with the progression of neurofibrillary degeneration in Alzheimer's disease
    Jin Jing Pei
    Karolinska Institutet, Neurotec, Division of Experimental Geriatrics, Novum, KFC Plan 4, Novum, S 141 86, Huddinge, Sweden
    Brain Res Mol Brain Res 109:45-55. 2002
    ..These data provide direct in situ evidence consistent with the possible involvement of MAP kinase pathway in the hyperphosphorylation of tau and the presence of this lesion before deposition of beta-amyloid in AD...
  30. ncbi alpha1 Integrin activation: a link between beta-amyloid deposition and neuronal death in aging hippocampal neurons
    Kelsi L Anderson
    Institute for Neuroscience, Northwestern University, Chicago, Illinois 60611, USA
    J Neurosci Res 75:688-97. 2004
    ..Taken collectively, these results identify alpha(1) integrin and the alpha(1) plus beta(1) integrin complexes as potential targets for therapeutic intervention in the Abeta signaling pathway in aging neurons...
  31. ncbi A mutation at codon 279 (N279K) in exon 10 of the Tau gene causes a tauopathy with dementia and supranuclear palsy
    M B Delisle
    Neuropathology Laboratory, INSERM U466, University Hospital, University Paul Sabatier, Toulouse, France
    Acta Neuropathol 98:62-77. 1999
    ..Our results suggest that the N279K mutation affects splicing similar to the intronic mutations, allowing exon 10 to be incorporated more frequently in the Tau transcript...
  32. ncbi [Diagnosis of and therapy for Alzheimer-type dementia]
    Yu Nakamura
    Seishin Shinkeigaku Zasshi 110:577-84. 2008
  33. ncbi beta-Amyloid protein aggregation: its implication in the physiopathology of Alzheimer's disease
    L Dumery
    UFR 927 des Sciences de la Vie, , 4 place Jussieu, 75252 Paris
    Pathol Biol (Paris) 49:72-85. 2001
    ..This review will focus on the current state of knowledge of A beta fibril formation, with special emphasis on physiological and exogenous inhibitors which may have a therapeutic potential...
  34. ncbi Distribution and dynamic process of neuronal cytoplasmic inclusion (NCI) in MSA: correlation of the density of NCI and the degree of involvement of the pontine nuclei
    T Yokoyama
    Department of Neurology, Kitazato University, School of Medicine, Kanagawa Rehabilitation Center, Japan
    Neuropathology 21:145-54. 2001
    ..Further systematic studies on NCI in the other brain regions are necessary to elucidate the pathogenesis of neuronal degeneration in MSA...
  35. ncbi The growth inhibitory factor that is deficient in the Alzheimer's disease brain is a 68 amino acid metallothionein-like protein
    Y Uchida
    Department of Neuropathology, Tokyo Metropolitan Institute of Gerontology, Japan
    Neuron 7:337-47. 1991
    ..In the AD cortex, the number of GIF-positive astrocytes was drastically reduced, suggesting that GIF is down-regulated in the subset of astrocytes during AD...
  36. ncbi Spatial patterns of alpha-synuclein positive glial cytoplasmic inclusions in multiple system atrophy
    Richard A Armstrong
    Vision Sciences, Aston University, Birmingham, United Kingdom
    Mov Disord 19:109-12. 2004
    ..These spatial patterns contrast with those reported for filamentous neuronal inclusions in the tauopathies and alpha-synucleinopathies...
  37. ncbi Polyglutamine and polyalanine expansions in ataxin7 result in different types of aggregation and levels of toxicity
    Morwena Latouche
    INSERM U679 former U289, Neurologie et Thérapeutique Expérimentale, Groupe Hospitalier Pitie Salpetriere, Paris, France
    Mol Cell Neurosci 31:438-45. 2006
    ....
  38. ncbi Clinical overview of the synucleinopathies
    Maria J Marti
    Movement Disorders Unit, Neurology Service, Institut Clinic de Malalties del Sistema Nervios, Hospital Clinic i Universitari, Barcelona, Spain
    Mov Disord 18:S21-7. 2003
    ..Clinicians should attempt to reach standard clinical diagnosis on patients, such as PD, PAF, or MSA...
  39. ncbi Divergent effects of the MEKK-1/JNK pathway on NB2a/d1 differentiation: some activity is required for outgrowth and stabilization of neurites but overactivation inhibits both phenomena
    Jason DeFuria
    Departments of Biological Sciences and Biochemistry, Center Cell Neurobiology and Neurodegeneration Research, University of Massachusetts, Lowell, Lowell, MA 01854, USA
    Brain Res 1123:20-6. 2006
    ..Finally, both caMEKK-1 and dnMEKK-1 prevented initial neuritogenesis. These findings indicate that the MEKK-1/JNK pathway regulates critical aspects of initial outgrowth, and subsequent stabilization of axonal neurites...
  40. ncbi TMAO promotes fibrillization and microtubule assembly activity in the C-terminal repeat region of tau
    Francesca Scaramozzino
    Department of Molecular, Cellular, and Developmental Biology, University of California, Santa Barbara, California 93106, USA
    Biochemistry 45:3684-91. 2006
    ..These studies set the stage for future high-resolution structural characterization of these intermediates and the basis by which Tyr(310) may direct pathologic versus normal tau function...
  41. ncbi Recent advances in experimental modeling of the assembly of tau filaments
    Li-Wen Ko
    Department of Neuroscience, Mayo Clinic Jacksonville, 4500 San Pablo Road, Jacksonville, FL 32224, USA
    Biochim Biophys Acta 1739:125-39. 2005
    ..This review highlights the latest developments in new models and how their utility improves our understanding of the sequence of events leading to human tauopathy...
  42. ncbi Peptides corresponding to gelsolin derived amyloid of the finnish type (AGelFIN) adopt two distinct forms in solution of which only one can polymerize into amyloid fibrils and form complexes with apoE
    Gibril O Fadika
    Amyloid 9:75-82. 2002
    ..Our results indicate that the amyloidogenic fragment of gelsolin can adopt two distinct forms, of which only one can form amyloid fibrils in vitro...
  43. ncbi A metallic impregnation technique adapted to study the honeybee Apis mellifera L. brain
    Luciana K Calabria
    Lab de Bioquímica e Biologia Molecular, Instituto de Genética e Bioquímica, Univ Federal de Uberlândia, Uberlandia, MG, Brazil, 38400 902
    Neotrop Entomol 39:720-4. 2010
    In order to visualize the distribution pattern of the neuronal bodies and neurofibrils in the honeybee brain, we adapted a metallic impregnation technique first described for vertebrate nervous system by Ramón y Cajal...
  44. ncbi Cajal's hypotheses on neurobiones and neurotropic factor match properties of microtubules and S-100 beta
    Efrain C Azmitia
    Departments of Biology and Psychiatry, Center for Neural Science, New York University, 100 Washington Square East, New York, NY 10003, USA
    Prog Brain Res 136:87-100. 2002
    ..the structure of neurons as composed of membrane, protoplasm, Golgi apparatus, nucleus, spongioplasm and neurofibrils (cytoskeleton)...
  45. ncbi Maturation of the neuromuscular junction in masseters of human fetus
    W Molina
    Department of Physiology, Faculty of Medicine, Universidad de Los Andes, Merida, Venezuela
    Rom J Morphol Embryol 51:537-41. 2010
    ..The aim of the present investigation is to examine if the histological maturation of the neuromuscular junction in the masseters of human fetuses has already begun by the 12-th week of gestation or not...
  46. ncbi Cajal's contribution to the knowledge of the neuronal cell nucleus
    Miguel Lafarga
    Department of Anatomy and Cell Biology and Centro de Investigación Biomédica en Red sobre Enferemedades Neurodegenerativas, University of Cantabria, Avd Cardenal Herrera Oria s n, 39011, Santander, Spain
    Chromosoma 118:437-43. 2009
    ..interest in intracellular neuronal structures and developed the reduced silver nitrate method for the study of neurofibrils (neurofilaments) and nuclear subcompartments...
  47. ncbi Infantile mitochondrial leucodystrophy - a case report
    Bogna Scmidt-Sidor
    Department of Neuropathology, Institute of Psychiatry and Neurology, Warszawa, Poland
    Folia Neuropathol 43:186-90. 2005
    ..The last one is characteristic of Leigh syndrome. Electron microscopic evaluation showed abnormal mitochondria, myelin and neurofibrils destruction. Hypertrophy of the heart may be also connected with mitochondrial disease.
  48. ncbi Sigmund Freud's contribution to the history of the neuronal cytoskeleton
    Eugenio Frixione
    Department of Cell Biology, and Department of Physiology, Biophysics and Neuroschiences, Center for Research and Advanced Studies IPN, Mexico City, Mexico
    J Hist Neurosci 12:12-24. 2003
    ..to this field is here examined in the context of the 19th-century debate regarding the existence of neurofibrils and of present views on the cytoskeleton...
  49. ncbi Rapid Bielschowsky silver impregnation method using microwave heating
    F Z Minbay
    Department of Histology and Embryology, Uludag University Faculty of Medicine, Bursa, Turkey
    Biotech Histochem 76:233-7. 2001
    ..impregnation method has been used extensively to demonstrate neuronal processes including dendrites, axons and neurofibrils. In this study, we examined the differences in the time required for and the staining quality of the ..
  50. ncbi René Couteaux (1909-1999) and the morphological identification of synapses
    Shigeru Tsuji
    Departement de Cytologie, Universite Pierre et Marie Curie, 7 quai Saint Bernard, 75005 Paris, France
    Biol Cell 98:503-9. 2006
    ..The discontinuity of the synaptic structure was confirmed by the three-dimensional observation of the intraneuronal network of neurofibrils with the first prototype of high-voltage electron microscope.
  51. ncbi [Structual changes of the apex region of the tongue in the elderly]
    Tomoko Takahashi
    Orofacial Pain Management, Department of Oral Restitution, Division of Oral Health Sciences, Graduate School, Tokyo Medical and Dental University
    Kokubyo Gakkai Zasshi 75:93-105. 2008
    ..involving morphological changes of layers, fibrosis, structural changes of myocytes and myofibrils, nerves and neurofibrils in this region...
  52. ncbi Bacopa monniera extract reduces amyloid levels in PSAPP mice
    Leigh A Holcomb
    Department of Psychiatry and Behavioral Science, Texas A and M, University System HSC College of Medicine, Temple, TX 76508, USA
    J Alzheimers Dis 9:243-51. 2006
    ..The areas encompassed by Congo Red-positive fibrillar amyloid deposits, however, were not altered by BME treatment. The data suggest that BME has potential application in Alzheimer's disease therapeutics...
  53. ncbi Anti-aggregation and fibril-destabilizing effects of sex hormones on alpha-synuclein fibrils in vitro
    Mie Hirohata
    Department of Neurology and Neurobiology of Aging, Kanazawa University Graduate School of Medical Science, Kanazawa 920 8640, Japan
    Exp Neurol 217:434-9. 2009
    ..These sex hormones, especially estriol, significantly exert anti-aggregation and fibril-destabilizing effects; and hence, could be valuable preventive and therapeutic agents for alpha-synucleinopathies...
  54. ncbi Abeta20-29 peptide blocking apoE/Abeta interaction reduces full-length Abeta42/40 fibril formation and cytotoxicity in vitro
    Jian Hao
    Department of Neurology, Tangdu Hospital, Fourth Military Medical University, Xi an City, Shaanxi Province, China
    Neuropeptides 44:305-13. 2010
    ..Our results raise the possibility that Abeta20-29 peptide blocking the interaction between full-length Abeta and apoE isoforms may be effective as a therapeutic agent for AD...
  55. ncbi Identification of synaptic plasma membrane proteins co-precipitated with fibrillar beta-amyloid peptide
    Yann Verdier
    Department of Medical Chemistry, University of Szeged, Szeged, Hungary
    J Neurochem 94:617-28. 2005
    ..Most of these proteins have already been associated with Alzheimer's disease, and the biological and pathophysiological significance of their interaction with fAbeta is discussed...
  56. ncbi Non-steroidal anti-inflammatory drugs have anti-amyloidogenic effects for Alzheimer's beta-amyloid fibrils in vitro
    Mie Hirohata
    Department of Neurology and Neurobiology of Aging, Kanazawa University Graduate School of Medical Science, Kanazawa 920-8640, Japan
    Neuropharmacology 49:1088-99. 2005
    ..Although the mechanisms by which these NSAIDs inhibit fA beta formation from A beta, and destabilize preformed fA beta in vitro are still unclear, NSAIDs may be promising for the prevention and treatment of AD...
  57. ncbi Axon cytoskeleton ultrastructure in chronic inflammatory demyelinating polyneuropathy
    Catherine Fressinaud
    Neurology Department, University Hospital, 4 rue Larrey, F49933 Angers Cedex 9, France
    Muscle Nerve 44:332-9. 2011
    ..To detail the extent and pattern of axon cytoskeleton alterations in chronic inflammatory demyelinating polyneuropathy (CIDP)...
  58. ncbi Histomorphological study of myelinated nerve fibres in the periodontal ligament of human canine
    Yan Huang
    Oral Imaging Center, Department of Dentistry, Oral Pathology and Maxillofacial Surgery, Faculty of Medicine, Catholic University of Leuven, Belgium
    Acta Odontol Scand 69:279-86. 2011
    ..This study aims to describe the human periodontal ligament (PDL) using serial sections, with a focus on mechanoreceptor distribution and morphology...
  59. ncbi Relationship between microtubule-binding repeats and morphology of neurofibrillary tangle in Alzheimer's disease
    T Kitamura
    Ishikawa Prefectural Takamatsu Hospital, Uchi-takamatsu, Kahoku, Ishikawa-ken, Japan
    Acta Neurol Scand 112:327-34. 2005
    ..CONCLUSIONS: Sectors CA2-CA4 showed predominantly 4R-NFT containing the pSer422 epitope. pSer262 may detect the process of transformation from p-NFT to i-NFT, and e-NFT consisted predominantly of 3R tau...
  60. ncbi Tau-dependent microtubule disassembly initiated by prefibrillar beta-amyloid
    Michelle E King
    Department of Biology, University of Virginia, Charlottesville, VA 22904, USA
    J Cell Biol 175:541-6. 2006
    ..These results suggest that a seminal cell biological event in AD pathogenesis is acute, tau-dependent loss of microtubule integrity caused by exposure of neurons to readily diffusible Abeta...
  61. ncbi Cajal's second great battle for the neuron doctrine: the nature and function of neurofibrils
    Eugenio Frixione
    Sección de Metodología y Teoría de la Ciencia, Centro de Investigación y de Estudios Avanzados CINVESTAV IPN, Apartado Postal 14 740, Mexico City, D F 07000 Mexico
    Brain Res Rev 59:393-409. 2009
    ..paradigm, championed by Stephan von Apáthy and Albrecht Bethe, held that nerve impulses propagate along neurofibrils connected in a continuous network throughout all nerve cells...
  62. ncbi Alzheimer neurofibrillary degeneration: significance, etiopathogenesis, therapeutics and prevention
    K Iqbal
    Department of Neurochemistry New York State Institute for Basic Research in Developmental Disabilities, Forest Hill Road, Staten Island, New York, NY 10314, USA
    J Cell Mol Med 12:38-55. 2008
    ..The AD subgroup identification of patients can help increase the success of clinical trials and the development of specific and potent disease modifying drugs...
  63. ncbi Preferential association of serum amyloid P component with fibrillar deposits in familial British and Danish dementias: similarities with Alzheimer's disease
    Agueda Rostagno
    Department of Pathology, New York University School of Medicine, New York 10016, USA
    J Neurol Sci 257:88-96. 2007
    ....
  64. ncbi Resveratrol prolongs lifespan and retards the onset of age-related markers in a short-lived vertebrate
    Dario R Valenzano
    Scuola Normale Superiore, 56100 Pisa, Italy
    Curr Biol 16:296-300. 2006
    ..These results demonstrate that food supplementation with resveratrol prolongs lifespan and retards the expression of age-dependent traits in a short-lived vertebrate...
  65. ncbi Hyperphosphorylated tau is a cause of neuronal dysfunction in tauopathy
    Akihiko Takashima
    Laboratory for Alzheimer s Disease, RIKEN Brain Science Institute, Wako Shi, Saitama, Japan
    J Alzheimers Dis 14:371-5. 2008
    ..Recent studies suggest that, before forming fibrils but after becoming hyperphosphorylated, tau is involved in neurodegenerative disease...
  66. ncbi The fate of axons subjected to traumatic ultrastructural (neurofilament) compaction: an electron-microscopic study
    Ferenc Gallyas
    Department of Neurosurgery, Faculty of Medicine, Pecs University, Ret utca 2, 7623, Pecs, Hungary
    Acta Neuropathol 111:229-37. 2006
    ..It is concluded that the non-recovering compacted axons undergo an uncommon (non-Wallerian) kind of degeneration, which is mostly reversible...
  67. ncbi [On the 100th anniversary of Alzheimer's disease]
    F R J Verhey
    Academisch Ziekenhuis Maastricht Alzheimer Centrum Limburg, afd Psychiatrie, Postbus 5800, 6202 AZ Maastricht
    Ned Tijdschr Geneeskd 150:2880-2. 2006
    ..patient with dementia who was found to have aggregated protein deposits (senile plaques) and abnormal neurofibrils in the cerebral cortex. Alzheimer was born in 1864 in Bavaria...
  68. ncbi Exploring the early steps of amyloid peptide aggregation by computers
    Normand Mousseau
    , , C.P. 6128, Succursale Centre-Ville, , , Canada
    Acc Chem Res 38:885-91. 2005
    ..We focus here on the structural and dynamic aspects of the aggregation as observed in state-of-the-art computer simulations of amyloid-forming peptides with an emphasis on the activation-relaxation technique...
  69. ncbi Inhibition of the formation of amyloid beta-protein fibrils using biocompatible nanogels as artificial chaperones
    Keisuke Ikeda
    Graduate School of Pharmaceutical Sciences, Kyoto University, Sakyo-ku, Kyoto, 606-8501, Japan
    FEBS Lett 580:6587-95. 2006
    ..In addition, CHPNH(2) nanogels protected PC12 cells from Abeta toxicity...
  70. ncbi Tau phosphorylation at threonine-175 leads to fibril formation and enhanced cell death: implications for amyotrophic lateral sclerosis with cognitive impairment
    May Gohar
    The Robarts Research Institute, The University of Western Ontario, London, Ontario, Canada
    J Neurochem 108:634-43. 2009
    ..Both tau fibril formation and cell death were significantly enhanced in the presence of Thr175-Asp-tau, regardless of the tau isoform, suggesting that phosphorylation of Thr175 is associated with tau fibril formation in ALSci...
  71. ncbi Preventing beta-amyloid fibrillization and deposition: beta-sheet breakers and pathological chaperone inhibitors
    Thomas Wisniewski
    Department of Neurology, New York University School of Medicine, 550 First Avenue, New York, NY 10016, USA
    BMC Neurosci 9:S5. 2008
    ..When combined with early pathology detection, these therapeutic strategies hold great promise as effective and relatively toxicity free methods of preventing AD related pathology...
  72. ncbi Inhibitory effect of minocycline on amyloid beta fibril formation and human microglial activation
    Atoosa Familian
    Department of Psychiatry, Institute for Clinical and Experimental Neurosciences VU ICEN VU, VU University Medical Center, Amsterdam, The Netherlands
    Glia 53:233-40. 2006
    ..Our data suggest that minocycline and tetracycline at tolerable doses can inhibit human microglial activation. This activity in part is exerted by inhibition of (SAP and C1q enhanced) Abeta fibril formation...
  73. ncbi Sensitive fluorescence polarization technique for rapid screening of alpha-synuclein oligomerization/fibrillization inhibitors
    Kelvin C Luk
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19143, USA
    Biochemistry 46:12522-9. 2007
    ..Thus, this FP method holds potential to accelerate discovery of disease modifying therapies for LB PD, DLB, and related neurodegenerative synucleinopathies...
  74. ncbi Pharmacological approaches of neurofibrillary degeneration
    Khalid Iqbal
    NYS Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, New York, 10314 USA. att.net
    Curr Alzheimer Res 2:335-41. 2005
    ..The development of drugs that inhibit neurofibrillary degeneration is a very promising and feasible therapeutic approach to inhibit the progression of AD and related tauopathies...
  75. ncbi Glial cells with differential neurite growth-modulating properties probed by atomic force microscopy
    G Weissmuller
    Instituto de Biofisica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, CCS B1 G Cidade Universitaria, 21949 900 Rio de Janeiro, Brazil
    Neurosci Res 38:217-20. 2000
    ....
  76. ncbi Mechanism of neurofibrillary degeneration and pharmacologic therapeutic approach
    K Iqbal
    New York State Institute for Basic Research in Developmental Disabilities, Staten Island 10314, USA
    J Neural Transm Suppl 59:213-22. 2000
    ..e. PHF/SF. Increase in tau phosphatase activity is a promising approach to inhibit neurofibrillary degeneration and thereby the diseases characterized by this lesion...
  77. ncbi Microtubule-associated protein tau, heparan sulphate and alpha-synuclein in several neurodegenerative diseases with dementia
    M G Spillantini
    MRC Brain Repair Centre and Department of Neurology, University of Cambridge, UK
    Acta Neuropathol 97:585-94. 1999
    ....
  78. ncbi NACP/alpha-synuclein immunoreactivity in fibrillary components of neuronal and oligodendroglial cytoplasmic inclusions in the pontine nuclei in multiple system atrophy
    K Arima
    Department of Ultrastructure and Histochemistry, Tokyo Institute of Psychiatry, Japan
    Acta Neuropathol 96:439-44. 1998
    ..The present study demonstrates that NACP is associated with cytoplasmic inclusions of MSA, and suggests a role of NACP in abnormal filament aggregation in neuronal degeneration...
  79. ncbi Neurofilaments are part of the high molecular weight complex containing neuronal cdc2-like kinase (nclk)
    K Y Lee
    Department of Anatomy, The University of Calgary, Alberta, Canada
    Brain Res 773:197-202. 1997
    ..These results are consistent with the formation of a functional macromolecular complex between nclk and neurofilaments in vivo and suggest a possible role for this kinase in regulating neuronal cytoskeletal networks...
  80. ncbi Glutamate AMPA receptors in the fascia dentata of human and kainate rat hippocampal epilepsy
    T L Babb
    Department of Neurosciences, Cleveland Clinic Foundation, OH 44195, USA
    Epilepsy Res 26:193-205. 1996
    ..Interestingly, the receptor upregulation precedes the mossy fiber ingrowth and may play a role in initiating axonal sprouting or in maintaining the aberrant mossy fiber synapses...
  81. ncbi Ultrastructural study of a perineurioma with ribosome-lamella complexes
    P Dhimes
    , Universidad Complutense de Madrid, Spain
    Ultrastruct Pathol 20:167-72. 1996
    ..Ultrastructurally, distinctive ribosome-lamella complexes were found in the cytoplasm of the perineurial cells. This may be the first time that these structures have been described in perineurioma...
  82. ncbi Hyperphosphorylation of tau in PHF
    M Morishima-Kawashima
    Department of Neuropathology, Faculty of Medicine, University of Tokyo, Japan
    Neurobiol Aging 16:365-71; discussion 371-80. 1995
    ..This extraphosphorylation may provide PHF-tau with the unusual characteristics including assembly incompetence...
  83. ncbi Quaking mouse: ultrastructural evidence for arrest of myelinogenesis
    H Wisniewski
    Brain Res 29:63-73. 1971
  84. ncbi Animal models of brain ageing and dementia
    M Sarter
    Research Laboratories of Schering AG, Berlin West, Federal Republic of Germany
    Compr Gerontol A 1:4-15. 1987
    ..and for their identification are discussed. In addition, the behavioral significance of each animal model is evaluated in the content of its meaning for cognitive alterations in senescence or in dementia...
  85. ncbi CNS amyloid proteins in neurodegenerative diseases
    G W Roberts
    Division of Psychiatry, Clinical Research Centre, Harrow, Middlesex, UK
    Neurology 38:1534-40. 1988
    ..Our results emphasize the need for classification of CNS amyloids based not on their morphology but on the macromolecular components comprising these pathologic polymers...
  86. ncbi Gerstmann-Sträussler-Scheinker disease. II. Neurofibrillary tangles and plaques with PrP-amyloid coexist in an affected family
    B Ghetti
    Department of Pathology Division of Neuropathology, Indiana University School of Medicine, Indianapolis 46202 5120
    Neurology 39:1453-61. 1989
    ....
  87. ncbi Multiple isoforms of human microtubule-associated protein tau: sequences and localization in neurofibrillary tangles of Alzheimer's disease
    M Goedert
    Medical Research Council, Laboratory of Molecular Biology, Cambridge, England
    Neuron 3:519-26. 1989
    ..Antisera raised against synthetic peptides corresponding to these different human tau isoforms demonstrate that multiple tau protein isoforms are incorporated into the neurofibrillary tangles of Alzheimer's disease...
  88. ncbi Sequence of a human MAP-2 region sharing epitopes with Alzheimer neurofibrillary tangles
    M Dammerman
    Department of Pathology, Albert Einstein College of Medicine, Bronx, New York 10461
    J Neurosci Res 24:487-95. 1989
    ..Expression vectors containing restriction fragments of the cDNA were used to assign the epitopes to a 51-amino-acid region near the end of the MAP-2 projection arm, distal to the microtubule...
  89. ncbi Galanin-like immunoreactivity is present in human substantia innominata and in senile plaques in Alzheimer's disease
    N W Kowall
    Neurology Service, Massachusetts General Hospital, Boston 02114
    Neurosci Lett 98:118-23. 1989
    ..The existence of galanin immunoreactivity in human magnocellular basal forebrain neurons which are depleted in Alzheimer's disease suggests that galanin may be similarly affected...
  90. ncbi [Alzheimer's neurofibrillary tangles in a 52-year-old patient with severe brain damage]
    Y Arai
    Department of Pediatrics, Tokyo Women's Medical College
    No To Hattatsu 22:602-7. 1990
    ..But the reason why NFT occur in this case is still obscure and probably different from that in the Down syndrome or in physiological senility...
  91. ncbi Apolipoprotein E immunoreactivity in cerebral amyloid deposits and neurofibrillary tangles in Alzheimer's disease and kuru plaque amyloid in Creutzfeldt-Jakob disease
    Y Namba
    Department of Neuropathology, Faculty of Medicine, University of Tokyo, Japan
    Brain Res 541:163-6. 1991
    ..The immunoreactivity was also found in amyloid of kuru plaques in Creutzfeldt-Jakob disease. Pretreatment of the sections with formic acid greatly enhanced immunoreactivity of senile and kuru plaques to antibody to apo E...
  92. ncbi Duodenal periampullary gangliocytic paraganglioma: report of two cases with immunohistochemical and ultrastructural study
    G Altavilla
    Institute of Pathological Anatomy and Histology, University of Padova, Italy
    Ultrastruct Pathol 25:137-45. 2001
    ..The histogenesis of GP is still a matter of debate, however its neoplastic nature is supported by the occasionally reported malignant evolution...
  93. ncbi Neuroarchitecture of the auditory cortex in the rufous horseshoe bat (Rhinolophus rouxi)
    S Radtke-Schuller
    Anatomische Anstalt, Ludwig Maximilians Universitat Munchen, Germany
    Anat Embryol (Berl) 204:81-100. 2001
    ..The accentuated neuroarchitectural features, like cortical thickness and staining intensity, are shown to coincide with the physiological representation of biologically significant parameters...
  94. ncbi The giant axonal neuropathy--clinical and hisotological aspects, differential diagnosis and a new case
    R Nafe
    Department of Neuroradiology, Johann Wolfgang Goethe University, Frankfurt/Main, Germany
    Clin Neuropathol 20:200-11. 2001
    ..Sporadic or familial cases with giant axons are discussed. Sceletal muscle biopsy (M. quadriceps femoris) showed neurogenic affection with presence of small angulated atrophic muscle fibres...
  95. ncbi Acetylcholinesterase in Hirschsprung's disease
    S W Moore
    Department of Paediatric Surgery, University of Stellenbosch, Cape Town, South Africa
    Pediatr Surg Int 21:255-63. 2005
    ..The presence of fine AChE neurofibrils in the ganglionated segment has contributed to the debate surrounding intestinal neuronal dysplasia...
  96. ncbi MARKing tau for tangles and toxicity
    Gerard Drewes
    Cellzome AG, Meyerhofstrasse 1, D 69117 Heidelberg, Germany
    Trends Biochem Sci 29:548-55. 2004
    ..Toxic consequences for the neuron might be exacerbated by tangle formation but are already evident during the early steps of the process...
  97. ncbi Prolactin-producing pituitary adenoma with incomplete neuronal transformation: an intermediate adenoma-neuronal tumor
    Eleni Thodou
    Departments of Pathology, 1G. Gennimatas General Hospital of Athens, KOFKA Building, 1st Floor, 154 Messogion Ave, 115 27, Athens, Greece
    Acta Neuropathol (Berl) 108:115-20. 2004
    ..Our case is the first PRL-producing pituitary adenoma showing incomplete neuronal differentiation lacking mature ganglion cells...
  98. ncbi Familial amyloidotic polyneuropathy: protein aggregation in the peripheral nervous system
    Maria João Saraiva
    Molecular Neurobiology, Instituto de Biologia Molecular e Celular, University of Porto, Portugal
    J Mol Neurosci 23:35-40. 2004
    ..They are pivotal for testing potential drugs for TTR amyloidosis as well...
  99. ncbi Mice overexpressing the human neurofilament heavy gene as a model of ALS
    J P Julien
    Centre for Research in Neuroscience, McGill University, Montreal General Hospital Research Institute, Canada
    Neurobiol Aging 16:487-90; discussion 490-2. 1995
    ..The relevance of the NF-H transgenics as a model of ALS is discussed in light of our current knowledge of motor neuron disease...
  100. ncbi Parkinson's syndrome associated with neurofibrillary degeneration and tau pathologic findings
    Andrew J Lees
    Reta Lila Weston Institute of Neurological Studies, University College London, Windeyer Medical Institute, London, United Kingdom
    Mov Disord 18:S28-33. 2003
    ..Further characterisation of these cases frequently confused with Parkinson's disease may broaden the clinical spectrum of parkinsonian disorders linked with neurofibrillary tangle formation...
  101. ncbi [CHANGE OF DENTAL PULP NERVES AND VESSELS IN VARIOUS STAGES OF CARIOUS PROCESSES IN MAN]
    E V ALEKSANDROVA
    Stomatologiia (Mosk) 44:23-7. 1965

Research Grants73

  1. The role of Mnbk in Downs Syndrome brain development and aging
    Jerzy Wegiel; Fiscal Year: 2007
    ..This study will provide a foundation for identifying the mechanisms and morphological substrate of specific functional deficits, and should contribute to the improvement of diagnosis and treatment. ..
  2. In Vivo Testing of Microtubule-Stabilizing Drugs in Triple Transgenic Mice
    MARY MICHAELIS; Fiscal Year: 2007
    ....
  3. Subgroups of Alzheimer Disease
    Khalid Iqbal; Fiscal Year: 2007
    ....
  4. Abnormal Hyperphosphorylation of Tau
    Khalid Iqbal; Fiscal Year: 2007
    ..The studies will lead also to the generation of a cellular and an animal model of tauopathies, which can be used for the development of therapeutic drugs for diseases characterized by this lesion. ..
  5. Therapeutic Targeting of Abnormal Conformation in Neurodegenerative Disease
    Thomas M Wisniewski; Fiscal Year: 2010
    ..The most toxic conformers are the oligomeric forms, which we plan to target by developing novel approaches to both increase their clearance and to reduce their toxicity. ..
  6. Modeling Neurofibrillary Degeneration
    Shu Hui Yen; Fiscal Year: 2007
    ..The results are likely to provide valuable information for a rational design of therapeutics to treat neurofibrillary degeneration. ..
  7. Amyloid beta Peptide and Apolipoprotein E
    Thomas Wisniewski; Fiscal Year: 2007
    ..These studies will test our central hypothesis that blocking the Aa/apoE interaction can serve as a novel, non-toxic therapeutic target for Alzheimer's disease. ..
  8. ADDLs, synapses & the molecular etiology of Alzheimer's disease
    WILLIAM KLEIN; Fiscal Year: 2007
    ..Successful completion of the project should identify new AD drug targets and provide mechanism-based assays for development of novel neuroprotective compounds useful for AD therapeutics. ..
  9. Progression of Tau Pathology in AD
    Lester Binder; Fiscal Year: 2007
    ..Using gene array technology, we propose to determine the relative quantities of CK1 message and the amounts of caspase message in individual CBF neurons from patients with the aforementioned clinical diagnoses. ..
  10. Amyloid and tau pathology in a transgenic model
    Michael Hutton; Fiscal Year: 2006
    ..abstract_text> ..
  11. Detection and Clearance of AD Amyloid Lesions
    Thomas Wisniewski; Fiscal Year: 2007
    ..Lay Summary: Active vaccination is an potential exciting therapy for AD; however, it can only be applied to patients if effective methods which are non-toxic can be developed. This application seeks to verify if this is possible. ..
  12. Membrane binding and aggregation of alpha-synuclein
    Jean Christophe Rochet; Fiscal Year: 2009
    ..Evidence that membrane-bound a-synuclein oligomers are valid drug targets would facilitate the development of screening assays to identify novel therapeutics. ..
  13. Tau Nitration and Oxidation in Alzheimer's Disease
    LESTER IRVIN BINDER; Fiscal Year: 2010
    ..We propose to determine the function of these alterations in disease and to determine when and where they occur. ..
  14. Abeta oligomers (ADDLs) in Alzheimer's Disease pathology
    William L Klein; Fiscal Year: 2010
    ..Results obtained with human ADDLs and tissue will help answer important questions central to ADDL involvement in pathogenesis and substantiate the targeting of ADDLs for future diagnostics and therapeutics. ..
  15. Detection and Clearance of AD Amyloid Lesions
    Thomas Wisniewski; Fiscal Year: 2009
    ..Lay Summary: Active vaccination is an potential exciting therapy for AD; however, it can only be applied to patients if effective methods which are non-toxic can be developed. This application seeks to verify if this is possible. ..
  16. ADDLs, synapses & the molecular etiology of Alzheimer's disease
    WILLIAM KLEIN; Fiscal Year: 2009
    ..Successful completion of the project should identify new AD drug targets and provide mechanism-based assays for development of novel neuroprotective compounds useful for AD therapeutics. ..
  17. Abeta oligomers (ADDLs) in Alzheimer's Disease pathology
    WILLIAM KLEIN; Fiscal Year: 2009
    ..Results obtained with human ADDLs and tissue will help answer important questions central to ADDL involvement in pathogenesis and substantiate the targeting of ADDLs for future diagnostics and therapeutics. ..
  18. Animal models for cerebral amyloid angiopathy
    Efrat Levy; Fiscal Year: 2006
    ..The proposed animal models are crucial for understanding the etiology of cerebral amyloid angiopathy and hemorrhage and for the development of rational therapeutic interventions. ..
  19. Detection and Clearance of AD Amyloid Lesions
    Thomas Wisniewski; Fiscal Year: 2006
    ..Our preliminary results indicate that APP/PS1 Tg aged mice have significant cognitive impairments versus controls. These studies will provide essential information before such approach can be safely used in humans. ..
  20. BETAAPP MODULATION BY THE ADAPTER PROTEINS FE65 AND X11
    Efrat Levy; Fiscal Year: 2003
    ..Manipulating the interaction of Beta-APP with an effector protein, such as X11 or Fe65, may provide a novel approach for the pharmacological modulation of Beta-APP processing in Alzheimer's disease. ..
  21. AMYLOID BETA PEPTIDE AND THEIR BINDING PROTEINS
    Thomas Wisniewski; Fiscal Year: 2002
    ..We will also identify if any of these labeled peptides are deposited on the Abeta lesions, in vivo. The latter could be used to develop a diagnostic test for AD. ..
  22. Abeta oligomers (ADDLs)in Alzheimers Disease pathology
    WILLIAM KLEIN; Fiscal Year: 2005
    ..abstract_text> ..
  23. The genetics of chromosome 17q21-linked tau-negative FTD
    Michael Hutton; Fiscal Year: 2006
    ..The identification of this gene will be a crucial step towards understanding the etiology of FTD as well as determining how this disease relates to MND. ..
  24. Assembly of tau filaments in cultured cells
    Michelle King; Fiscal Year: 2004
    ..abstract_text> ..
  25. Tau Nitration and Oxidation in Alzheimer's Disease
    Lester Binder; Fiscal Year: 2009
    ..We propose to determine the function of these alterations in disease and to determine when and where they occur. ..
  26. NEUROLOGICAL DEFICITS DUE TO TOXIC A BETA OLIGOMERS
    WILLIAM KLEIN; Fiscal Year: 2003
    ..In a best-case outcome, findings would provide novel targets for therapies that ultimately could reverse and not just slow down AD memory impairment. ..
  27. University of Kansas/Haskell Indian Nations University IRCDA Project
    MARY MICHAELIS; Fiscal Year: 2007
    ....