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 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
  2. 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
  3. 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
  4. 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
  5. pmc Calpain mediates calcium-induced activation of the erk1,2 MAPK pathway and cytoskeletal phosphorylation in neurons: relevance to Alzheimer's disease
    - Veeranna
    Center for Dementia Research, Nathan Kline Institute for Psychiatric Research, Orangeburg, New York, USA
    Am J Pathol 165:795-805. 2004
  6. 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
  7. 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
  8. 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
  9. 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
  10. 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

Detail Information

Publications117 found, 100 shown here

  1. 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...
  2. 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...
  3. 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
    ....
  4. 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...
  5. pmc Calpain mediates calcium-induced activation of the erk1,2 MAPK pathway and cytoskeletal phosphorylation in neurons: relevance to Alzheimer's disease
    - Veeranna
    Center for Dementia Research, Nathan Kline Institute for Psychiatric Research, Orangeburg, New York, USA
    Am J Pathol 165:795-805. 2004
    ....
  6. 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...
  7. 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...
  8. 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
  9. 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...
  10. 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...
  11. 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
    ....
  12. 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...
  13. 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...
  14. 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...
  15. 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...
  16. 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
  17. 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...
  18. 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...
  19. 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...
  20. 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
    ....
  21. 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
    ....
  22. 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...
  23. 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...
  24. 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...
  25. pmc 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
    ....
  26. pmc 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...
  27. ncbi [Diagnosis of and therapy for Alzheimer-type dementia]
    Yu Nakamura
    Seishin Shinkeigaku Zasshi 110:577-84. 2008
  28. 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...
  29. 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...
  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 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
    ....
  32. 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...
  33. 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...
  34. 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...
  35. 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...
  36. 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
    ....
  37. 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...
  38. 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...
  39. 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...
  40. 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...
  41. 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...
  42. 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...
  43. 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)...
  44. 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...
  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 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.
  47. 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 ..
  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 [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...
  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 Brain insulin resistance accelerates Aβ fibrillogenesis by inducing GM1 ganglioside clustering in the presynaptic membranes
    Naoki Yamamoto
    Laboratory of Neurochemistry, Department of Pharmacy, College of Pharmaceutical Sciences, Ritsumeikan University, Kusatsu, Shiga, Japan
    J Neurochem 121:619-28. 2012
    ....
  52. pmc Nucleotides released from Aβ₁₋₄₂ -treated microglial cells increase cell migration and Aβ₁₋₄₂ uptake through P2Y₂ receptor activation
    Hye Jung Kim
    Department of Biochemistry, University of Missouri, Columbia, Missouri, USA
    J Neurochem 121:228-38. 2012
    ..Taken together, our findings suggest that P2Y(2) Rs can activate microglial cells to enhance Aβ clearance and highlight the P2Y(2) R as a therapeutic target in Alzheimer's disease...
  53. pmc Amyloid β-protein aggregation produces highly reproducible kinetic data and occurs by a two-phase process
    Erik Hellstrand
    Chemistry Department and Molecular Protein Science, Lund University, P O Box 124, SE221 00 Lund, Sweden
    ACS Chem Neurosci 1:13-8. 2010
    ..0.2 μM, after which free Aβ decreased with total Aβ toward an asymptotic value. Our results imply that Aβ fibril formation arises from a sequence of events in a highly predictable manner...
  54. ncbi Age-related changes in Down syndrome brain and the cellular pathology of Alzheimer disease
    R S Williams
    Prog Brain Res 70:49-67. 1986
  55. 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...
  56. ncbi Ubiquitin is a component of neurofibrillary tangles in a variety of neurodegenerative diseases
    G Lennox
    Department of Neurology, University of Nottingham Medical School, Queen s Medical Centre, U K
    Neurosci Lett 94:211-7. 1988
    ..The observations suggest that ubiquitin may have an important role in the formation of neurofibrillary tangles in a variety of neurodegenerative diseases...
  57. 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...
  58. 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...
  59. 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
    ....
  60. 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...
  61. 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...
  62. pmc 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...
  63. 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
    ....
  64. 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...
  65. 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...
  66. 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...
  67. 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...
  68. 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...
  69. pmc 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...
  70. 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...
  71. ncbi Abnormal Tau proteins in progressive supranuclear palsy. Similarities and differences with the neurofibrillary degeneration of the Alzheimer type
    S Flament
    , Lille, France
    Acta Neuropathol 81:591-6. 1991
    ..The differences in the pathological Tau-variant profile that were observed between PSP and AD possibly reflect different etiopathogenetic pathways and might explain the formation of different types of filamentous Tau aggregates...
  72. pmc Pure akinesia: an atypical manifestation of progressive supranuclear palsy
    H Matsuo
    First Department of Internal Medicine, Nagasaki University, School of Medicine, Japan
    J Neurol Neurosurg Psychiatry 54:397-400. 1991
    ..At necropsy, pathological findings were not different from those reported for PSP. It is suggested that "pure akinesia" is an atypical manifestation of PSP, and that norepinephrinergic neurons may be involved in some types of PSP...
  73. doi 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)...
  74. doi 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...
  75. 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...
  76. 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...
  77. 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...
  78. 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...
  79. doi 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...
  80. 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...
  81. pmc 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...
  82. doi 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...
  83. 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...
  84. ncbi Quaking mouse: ultrastructural evidence for arrest of myelinogenesis
    H Wisniewski
    Brain Res 29:63-73. 1971
  85. 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...
  86. 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...
  87. 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...
  88. 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...
  89. ncbi Analysis of tauopathies with transgenic mice
    M Hutton
    Department of Neuroscience, Mayo Clinic, 4500 San Pablo Road, Jacksonville, FL, USA
    Trends Mol Med 7:467-70. 2001
    ..Recent progress in the development of transgenic mouse models of human tauopathy is allowing these questions to be addressed...
  90. ncbi Receptor for advanced glycation endproducts (RAGE) and the complications of diabetes
    David M Stern
    Department of Surgery, College of Physicians, Columbia University, P and S 17 401, West 168th Street, New York, NY 10032, USA
    Ageing Res Rev 1:1-15. 2002
    ....
  91. ncbi Human-specific organization of primary visual cortex: alternating compartments of dense Cat-301 and calbindin immunoreactivity in layer 4A
    Todd M Preuss
    University of Louisiana at Lafayette, Cognitive Evolution Group, New Iberia, LA 70560, USA
    Cereb Cortex 12:671-91. 2002
    ..The calbindin-rich compartments in human layer 4A cannot be related to a particular geniculostriate pathway on neurochemical grounds; they may constitute an interneuronal population that increased in human evolution...
  92. 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 108:115-20. 2004
    ..Our case is the first PRL-producing pituitary adenoma showing incomplete neuronal differentiation lacking mature ganglion cells...
  93. ncbi Role of long-range repulsive forces in organizing axonal neurofilament distributions: evidence from mice deficient in myelin-associated glycoprotein
    Sanjay Kumar
    Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    J Neurosci Res 68:681-90. 2002
    ..Among the models tested, a model in which the filaments interact through a long-range repulsive force is most consistent with the results of our analysis...
  94. ncbi Fibrillar inclusions and motor neuron degeneration in transgenic mice expressing superoxide dismutase 1 with a disrupted copper-binding site
    Jiou Wang
    Department of Neuroscience, Johns Hopkins School of Medicine, Baltimore, Maryland 21205, USA
    Neurobiol Dis 10:128-38. 2002
    ..Overall, our data are consistent with the hypothesis that the aberrant folding/aggregation of mutant SOD1 is a prominent feature in the pathogenesis of motor neuron disease...
  95. 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...
  96. ncbi APOE polymorphism and clinical duration determine regional neuropathology in Swedish APP(670, 671) mutation carriers: implications for late-onset Alzheimer's disease
    N Bogdanovic
    Neurotec, Geriatric Section, KI, Novum, KFC, Level 4, S 14186, Stockholm, Sweden
    J Cell Mol Med 6:199-214. 2002
    ..This raises the possibility that early Braak Stage I-II lesions might also follow this pattern of promotion...
  97. ncbi Genetic heterogeneity in giant axonal neuropathy: an Algerian family not linked to chromosome 16q24.1
    M Tazir
    Service de Neurologie, C H U Mustapha Bacha, Place du 1er Mai, 16000, Alger, Algeria
    Neuromuscul Disord 12:849-52. 2002
    ..We propose to call this form of giant axonal neuropathy giant axonal neuropathy 2, and to use the name of giant axonal neuropathy 1 for the form linked to 16q24.1...
  98. ncbi Oxidative stress precedes fibrillar deposition of Alzheimer's disease amyloid beta-peptide (1-42) in a transgenic Caenorhabditis elegans model
    Jennifer Drake
    Department of Chemistry and Center of Membrane Sciences, University of Kentucky, Lexington, KY 40506, USA
    Neurobiol Aging 24:415-20. 2003
    ..These results are discussed with reference to Alzheimer's disease...
  99. pmc Up-regulation of phosphorylated/activated p70 S6 kinase and its relationship to neurofibrillary pathology in Alzheimer's disease
    Wen Lin An
    Division of Experimental Geriatrics, Karolinska Institutet, Neurotec, Novum, Huddinge, Sweden
    Am J Pathol 163:591-607. 2003
    ..A p70 S6 kinase modulated up-regulation of tau translation might contribute to PHF-tau accumulation in neurons with neurofibrillary changes...
  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 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...

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
    ..unreadable] [unreadable]..
  3. GENOTYPE AND PHENOTYPE OF BRAINSTEM INJURY IN AUTISM
    Patricia Rodier; Fiscal Year: 1999
    ..for lacZ markers of Hoxa-1 expression, in situ hybridization for markers of the rhombomeres, and staining for neurofibrils. We shall develop animal models transgenic for human mutations involved in autism...
  4. GENOTYPE AND PHENOTYPE OF BRAINSTEM INJURY IN AUTISM
    Patricia Rodier; Fiscal Year: 2001
    ..for lacZ markers of Hoxa-1 expression, in situ hybridization for markers of the rhombomeres, and staining for neurofibrils. We shall develop animal models transgenic for human mutations involved in autism...
  5. GENOTYPE AND PHENOTYPE OF BRAINSTEM INJURY IN AUTISM
    Patricia Rodier; Fiscal Year: 2002
    ..for lacZ markers of Hoxa-1 expression, in situ hybridization for markers of the rhombomeres, and staining for neurofibrils. We shall develop animal models transgenic for human mutations involved in autism...
  6. GENOTYPE AND PHENOTYPE OF BRAINSTEM INJURY IN AUTISM
    Patricia Rodier; Fiscal Year: 2000
    ..for lacZ markers of Hoxa-1 expression, in situ hybridization for markers of the rhombomeres, and staining for neurofibrils. We shall develop animal models transgenic for human mutations involved in autism...
  7. GENOTYPE AND PHENOTYPE OF BRAINSTEM INJURY IN AUTISM
    Patricia Rodier; Fiscal Year: 2000
    ..for lacZ markers of Hoxa-1 expression, in situ hybridization for markers of the rhombomeres, and staining for neurofibrils. We shall develop animal models transgenic for human mutations involved in autism...
  8. GENOTYPE AND PHENOTYPE OF BRAINSTEM INJURY IN AUTISM
    Patricia Rodier; Fiscal Year: 2000
    ..for lacZ markers of Hoxa-1 expression, in situ hybridization for markers of the rhombomeres, and staining for neurofibrils. We shall develop animal models transgenic for human mutations involved in autism...
  9. GENOTYPE AND PHENOTYPE OF BRAINSTEM INJURY IN AUTISM
    Patricia Rodier; Fiscal Year: 2002
    ..for lacZ markers of Hoxa-1 expression, in situ hybridization for markers of the rhombomeres, and staining for neurofibrils. We shall develop animal models transgenic for human mutations involved in autism...
  10. GENOTYPE AND PHENOTYPE OF BRAINSTEM INJURY IN AUTISM
    Patricia Rodier; Fiscal Year: 2000
    ..for lacZ markers of Hoxa-1 expression, in situ hybridization for markers of the rhombomeres, and staining for neurofibrils. We shall develop animal models transgenic for human mutations involved in autism...
  11. ISOLATION AND CHARACTERIZATION OF THE PROTEOGLYCANS
    MOIRA BREEN; Fiscal Year: 1980
    ..to further our understanding of brain changes which have been observed in senility, such as "tangled neurofibrils", "reduced extracellular space" and the breakdown of intercellular communication which results in memory loss ..
  12. ABERRANT UBIQUITINYLATION IN AGED AND ALZHEIMER BRAIN
    Vincent Chau; Fiscal Year: 1990
    ..that brains from patients with Alzheimer's disease exhibit striking and unusual ubiquitin immunoreactivity on neurofibrils in regions containing NFT and SP...
  13. Subgroups of Alzheimer Disease
    Khalid Iqbal; Fiscal Year: 2007
    ....
  14. 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. ..
  15. 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. ..
  16. 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. [unreadable] [unreadable]..
  17. 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. ..
  18. 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. ..
  19. 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. ..
  20. Amyloid and tau pathology in a transgenic model
    Michael Hutton; Fiscal Year: 2006
    ..abstract_text> ..
  21. Amyloid beta Peptide and Apolipoprotein E
    Thomas Wisniewski; Fiscal Year: 2006
    ..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. ..
  22. Modeling Neurofibrillary Degeneration
    Shu Hui Yen; Fiscal Year: 2006
    ..The results are likely to provide valuable information for a rational design of therapeutics to treat neurofibrillary degeneration. [unreadable] [unreadable]..
  23. 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. ..
  24. Novel Hsp90 Inhibitors to Reduce Misfolded Proteins in Alzheimer's Disease
    MARY MICHAELIS; Fiscal Year: 2008
    ..Successful completion of this program will advance this concept toward clinical development. ..
  25. Membrane binding and aggregation of alpha-synuclein
    Jean Christophe Rochet; Fiscal Year: 2008
    ..Evidence that membrane-bound a-synuclein oligomers are valid drug targets would facilitate the development of screening assays to identify novel therapeutics. ..
  26. 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. ..
  27. 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. ..
  28. 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. ..
  29. 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. ..
  30. 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. ..
  31. 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. ..
  32. 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. ..
  33. University of Kansas/Haskell Indian Nations University IRCDA Project
    MARY MICHAELIS; Fiscal Year: 2008
    ....
  34. Detection and Clearance of AD Amyloid Lesions
    Thomas Wisniewski; Fiscal Year: 2008
    ..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. ..
  35. Therapeutic Approaches for Prion Disease
    Thomas Wisniewski; Fiscal Year: 2008
    ..In vivo imaging will also be done with 2 photon microscopy and non-toxic, Congo red analogs. Our novel imaging techniques will be used to monitor our therapeutic experiments. ..
  36. ADDLs, synapses & the molecular etiology of Alzheimer's disease
    WILLIAM KLEIN; Fiscal Year: 2008
    ..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. ..
  37. Amyloid beta Peptide and Apolipoprotein E
    Thomas Wisniewski; Fiscal Year: 2008
    ..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. ..
  38. Immunization Approaches for Alzheimer's Disease
    Thomas Wisniewski; Fiscal Year: 2008
    ..Vaccination is potentially an effective treatment, but is associated with significant toxicity in about 6% of patients. We propose studies to help develop safe, effective vaccines. [unreadable] [unreadable] [unreadable]..
  39. 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. ..
  40. 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. ..
  41. Amyloid and tau pathology in a transgenic model
    Michael Hutton; Fiscal Year: 2003
    ..abstract_text> ..
  42. 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. ..
  43. Animal models for cerebral amyloid angiopathy
    Efrat Levy; Fiscal Year: 2003
    ..The proposed animal models are crucial for understanding the etiology of cerebral amyloid angiopathy and hemorrhage and for the development of rational therapeutic interventions. ..
  44. Detection and Clearance of AD Amyloid Lesions
    Thomas Wisniewski; Fiscal Year: 2003
    ..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. ..
  45. 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. ..
  46. Tangle Formation in P301L Transgenic Mice
    Michael Hutton; Fiscal Year: 2002
    ....
  47. Detection and Clearance of AD Amyloid Lesions
    Thomas Wisniewski; Fiscal Year: 2002
    ..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. ..
  48. BETAAPP MODULATION BY THE ADAPTER PROTEINS FE65 AND X11
    Efrat Levy; Fiscal Year: 2001
    ..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. ..
  49. AMYLOID BETA PEPTIDE AND THEIR BINDING PROTEINS
    Thomas Wisniewski; Fiscal Year: 2001
    ..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. ..
  50. NEUROLOGICAL DEFICITS DUE TO TOXIC A BETA OLIGOMERS
    WILLIAM KLEIN; Fiscal Year: 2001
    ..In a best-case outcome, findings would provide novel targets for therapies that ultimately could reverse and not just slow down AD memory impairment. ..
  51. BETAAPP MODULATION BY THE ADAPTER PROTEINS FE65 AND X11
    Efrat Levy; Fiscal Year: 2000
    ..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. ..
  52. AMYLOID BETA PEPTIDE AND THEIR BINDING PROTEINS
    Thomas Wisniewski; Fiscal Year: 2000
    ..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. ..
  53. AMYLOID BETA PEPTIDE AND THEIR BINDING PROTEINS
    Thomas Wisniewski; Fiscal Year: 1999
    ..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. ..
  54. Detection and Clearance of AD Amyloid Lesions
    Thomas Wisniewski; Fiscal Year: 2004
    ..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. ..
  55. Animal models for cerebral amyloid angiopathy
    Efrat Levy; Fiscal Year: 2004
    ..The proposed animal models are crucial for understanding the etiology of cerebral amyloid angiopathy and hemorrhage and for the development of rational therapeutic interventions. ..
  56. Role of Mnbk in Downs Syndrome brain development & aging
    Jerzy Wegiel; Fiscal Year: 2004
    ..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. ..
  57. The role of Mnbk in DS brain development and aging
    Jerzy Wegiel; Fiscal Year: 2006
    ..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. ..
  58. Modeling Neurofibrillary Degeneration
    Shu Hui Yen; Fiscal Year: 2005
    ..The results are likely to provide valuable information for a rational design of therapeutics to treat neurofibrillary degeneration. ..
  59. Abeta oligomers (ADDLs)in Alzheimers Disease pathology
    WILLIAM KLEIN; Fiscal Year: 2005
    ..abstract_text> ..
  60. Therapeutic Approaches for Prion Disease
    Thomas Wisniewski; Fiscal Year: 2005
    ..In vivo imaging will also be done with 2 photon microscopy and non-toxic, Congo red analogs. Our novel imaging techniques will be used to monitor our therapeutic experiments. ..
  61. 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. [unreadable] [unreadable]..
  62. Detection and Clearance of AD Amyloid Lesions
    Thomas Wisniewski; Fiscal Year: 2005
    ..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. ..
  63. Assembly of tau filaments in cultured cells
    Michelle King; Fiscal Year: 2004
    ..abstract_text> ..
  64. Amyloid and tau pathology in a transgenic model
    Michael Hutton; Fiscal Year: 2004
    ..abstract_text> ..
  65. Animal models for cerebral amyloid angiopathy
    Efrat Levy; Fiscal Year: 2005
    ..The proposed animal models are crucial for understanding the etiology of cerebral amyloid angiopathy and hemorrhage and for the development of rational therapeutic interventions. ..
  66. Therapeutic Approaches for Prion Disease
    Thomas Wisniewski; Fiscal Year: 2006
    ..In vivo imaging will also be done with 2 photon microscopy and non-toxic, Congo red analogs. Our novel imaging techniques will be used to monitor our therapeutic experiments. ..
  67. Tangle Formation in P301L Transgenic Mice
    Michael Hutton; Fiscal Year: 2004
    ....
  68. The role of Mnbk in DS brain development and aging
    Jerzy Wegiel; Fiscal Year: 2005
    ..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. ..
  69. 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. ..
  70. Therapeutic Approaches for Prion Disease
    Thomas Wisniewski; Fiscal Year: 2004
    ..In vivo imaging will also be done with 2 photon microscopy and non-toxic, Congo red analogs. Our novel imaging techniques will be used to monitor our therapeutic experiments. ..
  71. 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. ..
  72. University of Kansas/Haskell Indian Nations University IRCDA Project
    MARY MICHAELIS; Fiscal Year: 2007
    ....