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. McKee A, Kosik K, Kowall N. Neuritic pathology and dementia in Alzheimer's disease. Ann Neurol. 1991;30:156-65 pubmed
    ..Widespread cerebral beta/A4 protein deposition may be necessary but by itself is insufficient for the development of dementia in AD. ..
  2. Mann D, Esiri M. The pattern of acquisition of plaques and tangles in the brains of patients under 50 years of age with Down's syndrome. J Neurol Sci. 1989;89:169-79 pubmed
  3. Kang J, Lemaire H, Unterbeck A, Salbaum J, Masters C, Grzeschik K, et al. The precursor of Alzheimer's disease amyloid A4 protein resembles a cell-surface receptor. Nature. 1987;325:733-6 pubmed
    ..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. ..
  4. Wisniewski K, Wisniewski H, Wen G. Occurrence of neuropathological changes and dementia of Alzheimer's disease in Down's syndrome. Ann Neurol. 1985;17:278-82 pubmed
    ..Plaques and tangles developed twenty to thirty years earlier and dementia was clinically detected at least three times more frequently (20 to 30%) in DS than it is known to occur in the non-DS population. ..
  5. Familian A, Boshuizen R, Eikelenboom P, Veerhuis R. Inhibitory effect of minocycline on amyloid beta fibril formation and human microglial activation. Glia. 2006;53:233-40 pubmed
    ..Our data suggest that minocycline and tetracycline at tolerable doses can inhibit human microglial activation. This activity in part is exerted by inhibition of (SAP and C1q enhanced) Abeta fibril formation. ..
  6. Levy E, Jaskolski M, Grubb A. The role of cystatin C in cerebral amyloid angiopathy and stroke: cell biology and animal models. Brain Pathol. 2006;16:60-70 pubmed
    ..This review focuses on cell culture and animal models used to study the role of cystatin C in these processes. ..
  7. Braak H, Braak E. Alzheimer's disease: striatal amyloid deposits and neurofibrillary changes. J Neuropathol Exp Neurol. 1990;49:215-24 pubmed
    ..Numerous argyrophilic threads in the neuropil were scattered throughout the nuclear gray matter. The striatum of non-demented individuals was virtually devoid of amyloid and neurofibrillary changes. ..
  8. Lomakin A, Teplow D, Kirschner D, Benedek G. Kinetic theory of fibrillogenesis of amyloid beta-protein. Proc Natl Acad Sci U S A. 1997;94:7942-7 pubmed
    ..We suggest that the method of QLS in combination with this theory can serve as a powerful tool for understanding the molecular factors that control Abeta plaque formation. ..
  9. Nixon R, Saito K, Grynspan F, Griffin W, Katayama S, Honda T, et al. Calcium-activated neutral proteinase (calpain) system in aging and Alzheimer's disease. Ann N Y Acad Sci. 1994;747:77-91 pubmed
    ..As a major effector of calcium signals, calpain activity may mirror disturbances in calcium homeostasis and mediate important pathologic consequences of such disturbances. ..

More Information

Publications62

  1. Julien J, Cote F, Collard J. Mice overexpressing the human neurofilament heavy gene as a model of ALS. Neurobiol Aging. 1995;16:487-90; discussion 490-2 pubmed
    ..The relevance of the NF-H transgenics as a model of ALS is discussed in light of our current knowledge of motor neuron disease. ..
  2. Scheper W, Hol E. Protein quality control in Alzheimer's disease: a fatal saviour. Curr Drug Targets CNS Neurol Disord. 2005;4:283-92 pubmed
    ..In this review, we will discuss the role of protein quality control in the neurotoxicity of Abeta. ..
  3. Skullerud K. Variations in the size of the human brain. Influence of age, sex, body length, body mass index, alcoholism, Alzheimer changes, and cerebral atherosclerosis. Acta Neurol Scand Suppl. 1985;102:1-94 pubmed
    ..In the majority of the cases, the Alzheimer changes were mild and had probably progressed slowly with age. A few cases had very severe changes.(ABSTRACT TRUNCATED AT 400 WORDS) ..
  4. Spires T, Orne J, Santacruz K, Pitstick R, Carlson G, Ashe K, et al. Region-specific dissociation of neuronal loss and neurofibrillary pathology in a mouse model of tauopathy. Am J Pathol. 2006;168:1598-607 pubmed
    ..Together, these results imply that neurofibrillary tangles do not necessarily lead to neuronal death. ..
  5. Horoupian D, Thal L, Katzman R, Terry R, Davies P, Hirano A, et al. Dementia and motor neuron disease: morphometric, biochemical, and Golgi studies. Ann Neurol. 1984;16:305-13 pubmed
    ..Because of severe degeneration of the substantia nigra in all three, the disease in these patients may represent a subset of motor neuron disease or a multisystem atrophy. ..
  6. Tellez Nagel I, Wisniewski H. Ultrastructure of neurofibrillary tangles in Steele-Richardson-Olszewski syndrome. Arch Neurol. 1973;29:324-7 pubmed
  7. Hammer R, Tomiyasu U, Scheibel A. Degeneration of the human Betz cell due to amyotrophic lateral sclerosis. Exp Neurol. 1979;63:336-46 pubmed
  8. Kreutz F, Frozza R, Breier A, de Oliveira V, Horn A, Pettenuzzo L, et al. Amyloid-? induced toxicity involves ganglioside expression and is sensitive to GM1 neuroprotective action. Neurochem Int. 2011;59:648-55 pubmed publisher
    ..This may be useful for designing new therapeutic strategies for Alzheimer's treatment. ..
  9. Ohm T, Braak H. Olfactory bulb changes in Alzheimer's disease. Acta Neuropathol. 1987;73:365-9 pubmed
    ..The tangle-bearing neurons of the olfactory bulb were identified as tufted cells, outer granule cells, and two different types of nerve cells forming the rostral part of the anterior olfactory nucleus. ..
  10. Serpell L, Blake C, Fraser P. Molecular structure of a fibrillar Alzheimer's A beta fragment. Biochemistry. 2000;39:13269-75 pubmed
    ..This detailed molecular structure of Abeta in its fibrous state provides clues as to the mechanism of amyloid assembly and identifies potential targets for controlling the aggregation process. ..
  11. Majocha R, Jungalwala F, Rodenrys A, Marotta C. Monoclonal antibody to embryonic CNS antigen A2B5 provides evidence for the involvement of membrane components at sites of Alzheimer degeneration and detects sulfatides as well as gangliosides. J Neurochem. 1989;53:953-61 pubmed
    ..The average level of sulfatides in AD brain was significantly higher than in normal controls. The data support the involvement of one or more membrane components with neurodegeneration in the Alzheimer brain. ..
  12. Lee K, Johnston R. Neurofilaments are part of the high molecular weight complex containing neuronal cdc2-like kinase (nclk). Brain Res. 1997;773:197-202 pubmed
    ..These results are consistent with the formation of a functional macromolecular complex between nclk and neurofilaments in vivo and suggest a possible role for this kinase in regulating neuronal cytoskeletal networks. ..
  13. Sarter M. Animal models of brain ageing and dementia. Compr Gerontol A. 1987;1:4-15 pubmed
    ..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. ..
  14. Altavilla G, Chiarelli S, Fassina A. Duodenal periampullary gangliocytic paraganglioma: report of two cases with immunohistochemical and ultrastructural study. Ultrastruct Pathol. 2001;25:137-45 pubmed
    ..The histogenesis of GP is still a matter of debate, however its neoplastic nature is supported by the occasionally reported malignant evolution. ..
  15. Lennox G, Lowe J, Morrell K, Landon M, Mayer R. Ubiquitin is a component of neurofibrillary tangles in a variety of neurodegenerative diseases. Neurosci Lett. 1988;94:211-7 pubmed
    ..The observations suggest that ubiquitin may have an important role in the formation of neurofibrillary tangles in a variety of neurodegenerative diseases. ..
  16. Sheng S. [Research progress on Alzheimer's disease: pathogenesis and medical therapy]. Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 2004;26:101-3 pubmed
    ..In this article, we discuss the mechanisms of AD in four aspects and put forward the strategies of drug therapy. ..
  17. Luk K, Hyde E, Trojanowski J, Lee V. Sensitive fluorescence polarization technique for rapid screening of alpha-synuclein oligomerization/fibrillization inhibitors. Biochemistry. 2007;46:12522-9 pubmed
    ..Thus, this FP method holds potential to accelerate discovery of disease modifying therapies for LB PD, DLB, and related neurodegenerative synucleinopathies. ..
  18. Chiba S, Takada E, Tadokoro M, Taniguchi T, Kadoyama K, Takenokuchi M, et al. Loss of dopaminoreceptive neuron causes L-dopa resistant parkinsonism in tauopathy. Neurobiol Aging. 2012;33:2491-505 pubmed publisher
    ..Interestingly, dopaminoreceptive (DAr) neurons in the striatum showed neurofibrils degeneration and apoptosis through caspase-3 activation by mutant tau accumulation...
  19. Tracz E, Dickson D, Hainfeld J, Ksiezak Reding H. Paired helical filaments in corticobasal degeneration: the fine fibrillary structure with NanoVan. Brain Res. 1997;773:33-44 pubmed
    ..The results suggest that 3-5-nm fibrils are the smallest structural subunits of filaments in CBD and that NanoVan may be an unique reagent in detecting eight-fibril organization in these less stable filaments. ..
  20. Dhimes P, Martinez Gonzalez M, Carabias E, Perez Espejo G. Ultrastructural study of a perineurioma with ribosome-lamella complexes. Ultrastruct Pathol. 1996;20:167-72 pubmed
    ..Ultrastructurally, distinctive ribosome-lamella complexes were found in the cytoplasm of the perineurial cells. This may be the first time that these structures have been described in perineurioma. ..
  21. Coria Balanzat F. [Advances in molecular pathology of Alzheimer's disease]. Rev Neurol. 2006;42:306-9 pubmed
    ..This series of events, known as the amyloid cascade, is supported by many genetic and experimental studies. ..
  22. Schultz C, Ghebremedhin E, Braak H, Braak E. Neurofibrillary pathology in the human paraventricular and supraoptic nuclei. Acta Neuropathol. 1997;94:99-102 pubmed
    ..The alterations in the paraventricular and supraoptic nuclei were consistently accompanied by neurofibrillary changes in the mediobasal hypothalamus. ..
  23. Stone J, Peterson A, Eyer J, Oblak T, Sickles D. Neurofilaments are nonessential to the pathogenesis of toxicant-induced axonal degeneration. J Neurosci. 2001;21:2278-87 pubmed
    ..These results also suggest that the role of neurofilament accumulation in the pathogenesis of neurodegenerative diseases requires careful evaluation. ..
  24. Uchida Y, Takio K, Titani K, Ihara Y, Tomonaga M. The growth inhibitory factor that is deficient in the Alzheimer's disease brain is a 68 amino acid metallothionein-like protein. Neuron. 1991;7:337-47 pubmed
    ..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. ..
  25. Marti M, Tolosa E, Campdelacreu J. Clinical overview of the synucleinopathies. Mov Disord. 2003;18 Suppl 6:S21-7 pubmed
    ..Clinicians should attempt to reach standard clinical diagnosis on patients, such as PD, PAF, or MSA. ..
  26. Hong H, Rana S, Barrigan L, Shi A, Zhang Y, Zhou F, et al. Inhibition of Alzheimer's amyloid toxicity with a tricyclic pyrone molecule in vitro and in vivo. J Neurochem. 2009;108:1097-1108 pubmed publisher
    ..Our results suggest that CP2 might be beneficial to AD patients by preventing Abeta aggregation and disaggregating existing Abeta oligomers and protofibrils. ..
  27. Tandan R, Bradley W. Amyotrophic lateral sclerosis: Part 1. Clinical features, pathology, and ethical issues in management. Ann Neurol. 1985;18:271-80 pubmed
  28. King M, Kan H, Baas P, Erisir A, Glabe C, Bloom G. Tau-dependent microtubule disassembly initiated by prefibrillar beta-amyloid. J Cell Biol. 2006;175:541-6 pubmed
    ..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. ..
  29. Gallyas F, Pal J, Farkas O, Doczi T. The fate of axons subjected to traumatic ultrastructural (neurofilament) compaction: an electron-microscopic study. Acta Neuropathol. 2006;111:229-37 pubmed
    ..It is concluded that the non-recovering compacted axons undergo an uncommon (non-Wallerian) kind of degeneration, which is mostly reversible. ..
  30. Soto C, Saborio G, Permanne B. Inhibiting the conversion of soluble amyloid-beta peptide into abnormally folded amyloidogenic intermediates: relevance for Alzheimer's disease therapy. Acta Neurol Scand Suppl. 2000;176:90-5 pubmed
    ..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. ..
  31. Tomlinson B, Irving D, Blessed G. Cell loss in the locus coeruleus in senile dementia of Alzheimer type. J Neurol Sci. 1981;49:419-28 pubmed
    ..Some evidence exists that the more severe cases of SDAT in terms of neocortical plaque formation have the greatest loss of LC neurons. ..
  32. Fadika G, Baumann M. 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. Amyloid. 2002;9:75-82 pubmed
    ..Our results indicate that the amyloidogenic fragment of gelsolin can adopt two distinct forms, of which only one can form amyloid fibrils in vitro. ..
  33. Bondareff W, Mountjoy C, Roth M. Selective loss of neurones of origin of adrenergic projection to cerebral cortex (nucleus locus coeruleus) in senile dementia. Lancet. 1981;1:783-4 pubmed
  34. Schochet S, Lampert P, Earle K. Alexander's disease. A case report with electron microscopic observations. Neurology. 1968;18:543-9 pubmed
  35. Wang J, Xia Y, Grundke Iqbal I, Iqbal K. Abnormal hyperphosphorylation of tau: sites, regulation, and molecular mechanism of neurofibrillary degeneration. J Alzheimers Dis. 2013;33 Suppl 1:S123-39 pubmed
    ..In this article we briefly review the progress made in these areas of research. ..
  36. Oien D, Shinogle H, Moore D, Moskovitz J. Clearance and phosphorylation of alpha-synuclein are inhibited in methionine sulfoxide reductase a null yeast cells. J Mol Neurosci. 2009;39:323-32 pubmed publisher
    ..Thus, a compromised MsrA function combined with alpha-synuclein overexpression may promote processes leading to synucleinopathies. ..
  37. Bugiani O, Mancardi G, Brusa A, Ederli A. The fine structure of subcortical neurofibrillary tangles in progressive supranuclear palsy. Acta Neuropathol. 1979;45:147-52 pubmed
  38. Flament S, Delacourte A, Hemon B, Defossez A. Characterization of two pathological tau protein, variants in Alzheimer brain cortices. J Neurol Sci. 1989;92:133-41 pubmed
    ..Consequently, they might appear before the lesions and might be instrumental for the search of biochemical deregulations that precede the neurofibrillary degeneration. ..
  39. Tanev I, Tanev V. [Correlation between changes in the nerve fiber layer and examination of the visual field using automatic perimetry in diagnosing primary open angle glaucoma]. J Fr Ophtalmol. 2002;25:936-9 pubmed
    ..Thus it will be possible to save time for: early diagnosis, monitoring the treatment, limiting the progression of glaucoma. ..
  40. Zatta P, Zambenedetti P, Stella M, Licastro F. Astrocytosis, microgliosis, metallothionein-I-II and amyloid expression in high cholesterol-fed rabbits. J Alzheimers Dis. 2002;4:1-9 pubmed
    ..The relevance on the cholesterol metabolism in Alzheimer's disease pathogenesis is also discussed. ..
  41. Gallyas F. Silver staining of Alzheimer's neurofibrillary changes by means of physical development. Acta Morphol Acad Sci Hung. 1971;19:1-8 pubmed
  42. Klein W. ADDLs & protofibrils--the missing links?. Neurobiol Aging. 2002;23:231-5 pubmed
  43. Wegiel J, Dowjat K, Kaczmarski W, Kuchna I, Nowicki K, Frackowiak J, et al. The role of overexpressed DYRK1A protein in the early onset of neurofibrillary degeneration in Down syndrome. Acta Neuropathol. 2008;116:391-407 pubmed publisher
  44. Shen S, Zhao Y, Yang W, Xu L, Sun Z, Chen X, et al. Decreased nerve distribution in mixed venous-lymphatic malformation. Int J Oral Maxillofac Surg. 2008;37:1106-10 pubmed publisher
    ..These data suggest that the decreased distribution of sensory nerve fibers in MVLMs may be involved in the pathogenesis of MVLM of the tongue. ..
  45. Jouhilahti E, Visnapuu V, Soukka T, Aho H, Peltonen S, Happonen R, et al. Oral soft tissue alterations in patients with neurofibromatosis. Clin Oral Investig. 2012;16:551-8 pubmed publisher
    ..The clinicians should recognize that oral soft tissue alterations are relatively common in NF1. Some of the growths are disturbing, and plexiform neurofibromas may bear a risk of malignant transformation. ..
  46. Harrington C, Mukaetova Ladinska E, Hills R, Edwards P, Montejo De Garcini E, Novak M, et al. Measurement of distinct immunochemical presentations of tau protein in Alzheimer disease. Proc Natl Acad Sci U S A. 1991;88:5842-6 pubmed
  47. Liem R, Yen S, Salomon G, Shelanski M. Intermediate filaments in nervous tissues. J Cell Biol. 1978;79:637-45 pubmed
    ..These results indicate that neurofilaments and glial filaments are composed of different polypeptides and have different solubility characteristics. ..
  48. Agorogiannis E, Agorogiannis G, Papadimitriou A, Hadjigeorgiou G. Protein misfolding in neurodegenerative diseases. Neuropathol Appl Neurobiol. 2004;30:215-24 pubmed
  49. Ikeda K, Okada T, Sawada S, Akiyoshi K, Matsuzaki K. Inhibition of the formation of amyloid beta-protein fibrils using biocompatible nanogels as artificial chaperones. FEBS Lett. 2006;580:6587-95 pubmed
    ..In addition, CHPNH(2) nanogels protected PC12 cells from Abeta toxicity. ..
  50. Tomonaga M. Neuropathology of the locus ceruleus: a semi-quantitative study. J Neurol. 1983;230:231-40 pubmed
    ..Lewy bodies and neurofibrillary tangles appeared increasingly in old age. However, the incidence of both changes in the same neuron was rare, and in such cases their structures appeared not to be related. ..
  51. Frixione E. Neura, nerves, nerve fibers, neurofibrils, microtubules: multidimensional routes of pain, pleasure, and voluntary action in images across the ages. Prog Brain Res. 2013;203:115-60 pubmed publisher
    ..And every step has been a source of amazing imagery. ..
  52. Gohar M, Yang W, Strong W, Volkening K, Leystra Lantz C, Strong M. Tau phosphorylation at threonine-175 leads to fibril formation and enhanced cell death: implications for amyotrophic lateral sclerosis with cognitive impairment. J Neurochem. 2009;108:634-43 pubmed publisher
    ..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. ..
  53. Dickson D, Farlo J, Davies P, Crystal H, Fuld P, Yen S. Alzheimer's disease. A double-labeling immunohistochemical study of senile plaques. Am J Pathol. 1988;132:86-101 pubmed