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. 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
  2. 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
  3. 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
  4. 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
  5. 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
  6. 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
  7. 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
  8. 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
  9. 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
  10. 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

Research Grants

Detail Information

Publications140 found, 100 shown here

  1. 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
    ....
  2. 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
    ....
  3. 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...
  4. 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...
  5. 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
    ....
  6. 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...
  7. 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...
  8. 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
    ....
  9. 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...
  10. 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...
  11. 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...
  12. 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...
  13. 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...
  14. 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
  15. 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
    ....
  16. 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...
  17. 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...
  18. 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...
  19. 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...
  20. 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...
  21. 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...
  22. 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...
  23. 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...
  24. 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...
  25. 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)...
  26. 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...
  27. 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.
  28. 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...
  29. 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 ..
  30. 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...
  31. 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.
  32. 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...
  33. pmc A fibril-specific, conformation-dependent antibody recognizes a subset of Abeta plaques in Alzheimer disease, Down syndrome and Tg2576 transgenic mouse brain
    Floyd Sarsoza
    Institute for Brain Aging and Dementia, University of California, Irvine, CA 92697, USA
    Acta Neuropathol 118:505-17. 2009
    ....
  34. ncbi Gonadotropin-inhibitory hormone promoter-driven enhanced green fluorescent protein expression decreases during aging in female rats
    Tomoko Soga
    Brain Research Institute T S, T K, I S P, School of Medicine and Health Sciences, Monash University, Sunway, PJ 46150, Malaysia and Department of Physiology I J C, Monash University, Victoria 3880, Australia
    Endocrinology 155:1944-55. 2014
    ..We conclude that there is an age-related decline in GnIH neuron number and GnIH inputs to GnRH neurons. We also conclude that the response of GnIH neurons to estrogen diminishes with reproductive aging. ..
  35. 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...
  36. ncbi Cerebrospinal fluid from patients with multiple system atrophy promotes in vitro α-synuclein fibril formation
    Mie Hirohata
    Department of Neurology and Neurobiology of Aging, Kanazawa University Graduate School of Medical Science, Kanazawa 920 8640, Japan
    Neurosci Lett 491:48-52. 2011
    ..By electron microscopic analyses, the width of fαS formed in MSA-CSF was significantly greater than others. MSA may have a CSF environment particularly favorable for fαS formation...
  37. ncbi Ontogenic attendance of neuropeptides in the embryo chicken retina
    J A Prada Oliveira
    Department of Human Anatomy and Embryology, Faculty of Medicine, University of Cadiz, Cadiz, Spain
    Histol Histopathol 18:1013-26. 2003
    ..Their presence may indicate roles as neuronal differentiation or growth factors...
  38. ncbi [Diagnosis of and therapy for Alzheimer-type dementia]
    Yu Nakamura
    Seishin Shinkeigaku Zasshi 110:577-84. 2008
  39. 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...
  40. 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...
  41. 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...
  42. 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
    ....
  43. 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
    ....
  44. 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...
  45. ncbi Neura, nerves, nerve fibers, neurofibrils, microtubules: multidimensional routes of pain, pleasure, and voluntary action in images across the ages
    Eugenio Frixione
    Section of Methodology and Theory of Science, Department of Cell Biology, Center for Research and Advanced Studies IPN Cinvestav, Mexico City, Mexico Electronic address
    Prog Brain Res 203:115-60. 2013
    ..And every step has been a source of amazing imagery. ..
  46. ncbi Neuronal damage in hydrocephalus and its restoration by shunt insertion in experimental hydrocephalus: a study involving the neurofilament-immunostaining method
    Yuichi Aoyama
    Departments of Neurosurgery and Surgical Pathology, University of Occupational and Environmental Health, Kitakyushu, Japan
    J Neurosurg 104:332-9. 2006
    ....
  47. 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...
  48. 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...
  49. ncbi Hypomyelination in the quaking mouse. A model for the analysis of disturbed myelin formation
    T Samorajski
    J Neuropathol Exp Neurol 29:507-23. 1970
  50. pmc Inhibition of fibril formation in beta-amyloid peptide by a novel series of benzofurans
    D R Howlett
    Department of Neuroscience, SmithKline Beecham Pharmaceuticals, New Frontiers Science Park North, Third Avenue, Harlow, Essex CM19 5AW, UK
    Biochem J 340:283-9. 1999
    ..Thus a specific recognition site might exist for benzofurans on beta-amyloid, binding to which seems to interfere with the ability of the peptide to form fibrils...
  51. ncbi PD98059 prevents neurite degeneration induced by fibrillar beta-amyloid in mature hippocampal neurons
    M Rapoport
    Institute for Neuroscience, Northwestern University, Chicago, Illinois 60611, USA
    J Neurochem 74:125-33. 2000
    ..Taken collectively, our results suggest that the sustained activation of the MAPK signal transduction pathway induced by fibrillar Abeta may lead to the abnormal phosphorylation of tau and the neuritic degeneration observed in AD...
  52. ncbi Immunohistochemical and ultrastructural characterization of ubiquitinated eosinophilic fibrillary neuronal inclusions in sporadic amyotrophic lateral sclerosis
    K Arima
    Department of Ultrastructure and Histochemistry, Tokyo Institute of Psychiatry, Japan
    Acta Neuropathol 96:75-85. 1998
    ....
  53. ncbi Furin mediates enhanced production of fibrillogenic ABri peptides in familial British dementia
    S H Kim
    Department of Neurobiology, Pharmacology and Physiology, The University of Chicago, Abbott 316, 947 East 58th Street, Chicago, Illinois 60637, USA
    Nat Neurosci 2:984-8. 1999
    ..Collectively, our results support the view that enhanced furin-mediated processing of mutant BRI generates fibrillogenic peptides that initiate the pathogenesis of FBD...
  54. ncbi Neurofilaments are nonessential to the pathogenesis of toxicant-induced axonal degeneration
    J D Stone
    Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta, Georgia 30912, USA
    J Neurosci 21:2278-87. 2001
    ..These results also suggest that the role of neurofilament accumulation in the pathogenesis of neurodegenerative diseases requires careful evaluation...
  55. 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...
  56. ncbi Quantitative and electron microscopic studies of sensory ganglion cells of the Sprawling mouse
    L W Duchen
    J Neurocytol 6:465-81. 1977
    ..Reconstructions from serial sections showed that ganglion cells in Swl were highly irregular in shape...
  57. 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
  58. pmc Intermediate filaments in nervous tissues
    R K Liem
    J Cell Biol 79:637-45. 1978
    ..These results indicate that neurofilaments and glial filaments are composed of different polypeptides and have different solubility characteristics...
  59. 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...
  60. pmc Monoclonal antibody binding to congophilic elements in human Alzheimer brain
    S M MacDonald
    J Clin Pathol 39:1199-203. 1986
    ..This antibody reacts with dendritic reticulum cells in lymph node and tonsil, and, in Alzheimer brain, with argyrophilic plaques, neurofibrillary tangles, and cerebral vascular amyloid...
  61. 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
    ....
  62. 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...
  63. 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...
  64. pmc Heme oxygenase-1 is associated with the neurofibrillary pathology of Alzheimer's disease
    M A Smith
    Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106
    Am J Pathol 145:42-7. 1994
    ....
  65. ncbi Inhibitory neurons from fetal rat cerebral cortex exert delayed axon formation and active migration in vitro
    Kensuke Hayashi
    Department of Cell Biology, Institute for Molecular and Cellular Regulation, Gunma University, 3 39 15 Showamachi, Maebashi, Gunma 371 8512, Japan
    J Cell Sci 116:4419-28. 2003
    ..Inhibitory neurons thus possess a more effective cytoskeletal machinery for migration than excitatory neurons and they form axons later...
  66. ncbi Inhibiting the conversion of soluble amyloid-beta peptide into abnormally folded amyloidogenic intermediates: relevance for Alzheimer's disease therapy
    C Soto
    Serono Pharmaceutical Research Institute, Geneva, Switzerland
    Acta Neurol Scand Suppl 176:90-5. 2000
    ..It remains to be proved that inhibition of the defective folding of amyloid-beta peptide and/or amyloid plaque deposition could be beneficial for the therapeutic treatment of Alzheimer's disease...
  67. ncbi Acute and delayed implantation of positively charged 2-hydroxyethyl methacrylate scaffolds in spinal cord injury in the rat
    Ales Hejcl
    Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Czech Republic
    J Neurosurg Spine 8:67-73. 2008
    ..Hydrogels are nontoxic, chemically inert synthetic polymers with a high water content and large surface area that provide mechanical support for cells and axons when implanted into spinal cord tissue...
  68. ncbi Modulation of PHF-like tau phosphorylation in cultured neurones and transfected cells
    B H Anderton
    Department of Neuroscience, Institute of Psychiatry, London, United Kingdom
    Neurobiol Aging 16:389-97; discussion 398-402. 1995
    ..These results suggest that aberrant regulation of GSK-3 alpha/beta may be a pathogenic mechanism in Alzheimer's disease...
  69. ncbi [Correlation between changes in the nerve fiber layer and examination of the visual field using automatic perimetry in diagnosing primary open angle glaucoma]
    I Tanev
    Service d Ophtalmologie, Université Médicale, 49, boulevard Evlogi Georgiev, 1142 Sofia, Bulgarie
    J Fr Ophtalmol 25:936-9. 2002
    ..To analyse the correlation between changes in the nerve fiber layer and the appearance of defects in the visual field in primary open angle glaucoma (POAG)...
  70. 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...
  71. ncbi Neurofilaments consist of distinct populations that can be distinguished by C-terminal phosphorylation, bundling, and axonal transport rate in growing axonal neurites
    J T Yabe
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts-Lowell, Lowell, Massachusetts 01854, USA
    J Neurosci 21:2195-205. 2001
    ..Inhibition of phosphatase activities increased NF-NF interactions within living cells. These findings collectively suggest that C-terminal phosphorylation and NF-NF interactions are responsible for slowing NF axonal transport...
  72. 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...
  73. ncbi [Drug development for tauopathy and Alzheimer's disease]
    Akihiko Takashima
    Brain Science Institute, RIKEN, Wako, Japan
    Nihon Shinkei Seishin Yakurigaku Zasshi 30:177-80. 2010
    ..Therefore, inhibition of oligomer tau, and granular tau aggregation is expected to block the progression of AD symptoms by preventing synapse loss and neuronal loss...
  74. 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
  75. 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...
  76. 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...
  77. 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...
  78. 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...
  79. 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
    ....
  80. 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...
  81. 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...
  82. 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...
  83. 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...
  84. 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...
  85. 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)...
  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 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...
  88. 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...
  89. 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...
  90. 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...
  91. 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...
  92. 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
    ....
  93. 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...
  94. 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...
  95. 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...
  96. 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...
  97. 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...
  98. 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...
  99. 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...
  100. 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...
  101. 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...

Research Grants22

  1. In Vivo Testing of Microtubule-Stabilizing Drugs in Triple Transgenic Mice
    MARY MICHAELIS; Fiscal Year: 2007
    ..unreadable] [unreadable]..
  2. 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...
  3. 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...
  4. 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 ..
  5. The role of Mnbk in Downs Syndrome brain development and aging
    Jerzy Wegiel; Fiscal Year: 2008
    ..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. ..
  6. The assembly of characterization of tau oligomers
    Michelle King; Fiscal Year: 2006
    ..Together, the aims of this study will facilitate a greater understanding of tau filaments and tau filament assembly in a number of neurodegenerative diseases including Alzheimer's Disease. ..
  7. Modeling Neurofibrillary Degeneration
    Shu Hui Yen; Fiscal Year: 2008
    ..The results are likely to provide valuable information for a rational design of therapeutics to treat neurofibrillary degeneration. [unreadable] [unreadable]..
  8. Tangle Formation in P301L Transgenic Mice
    Michael Hutton; Fiscal Year: 2005
    ....
  9. Amyloid beta Peptide and Apolipoprotein E
    Thomas Wisniewski; Fiscal Year: 2009
    ..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. ..
  10. Antioxidant function of MsrA in dopaminergic neurons
    Jean Christophe Rochet; Fiscal Year: 2007
    ..In turn, this information may stimulate the development of new therapeutic approaches in the treatment of age-related diseases of the brain. [unreadable] [unreadable]..
  11. 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. ..
  12. 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. ..
  13. 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]..
  14. 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. ..
  15. 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. ..
  16. Amyloid and tau pathology in a transgenic model
    Michael Hutton; Fiscal Year: 2006
    ..abstract_text> ..
  17. 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. ..
  18. Assembly of tau filaments in cultured cells
    Michelle King; Fiscal Year: 2004
    ..abstract_text> ..
  19. 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. ..
  20. 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. ..
  21. 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. ..