Accès gratuit
Numéro
Med Sci (Paris)
Volume 18, Numéro 6-7, Juin–Juillet 2002
Page(s) 727 - 736
Section M/S Revues : Articles de Synthèse
DOI https://doi.org/10.1051/medsci/20021867727
Publié en ligne 15 juin 2002
  1. Alzheimer A. Über eine eigenartige erkrankung der hirnrinde. Allg Z Psychiat 1907; 64 : 146–8. [Google Scholar]
  2. Glenner GG, Wong CW. Alzheimer’s disease : initial report of the purification and characterization of a novel cerebrovascular amyloid protein. Biochem Biophys Res Commun 1984; 120 : 885–90. [Google Scholar]
  3. Brion JP, Passareiro H, Nunez J, Flament-Durand J. Immunological determinants of tau proteins are present in neurofibrillary tangles of Alzheimer’s disease. Arch Biol (Brux) 1985; 95 : 229–35. [Google Scholar]
  4. Lee VMY, Goedert M, Trojanowski JQ. Neurodegenerative tauopathies. Ann Rev Neurosci 2001; 24 : 1121–59. [Google Scholar]
  5. Delacourte A, Buée L. Tau pathology : a marker of neurodegenerative disorders. Curr Opin Neurol 2000; 13 : 371–6. [Google Scholar]
  6. Biernat J, Gustke N, Drewes G, Mandelkow EM, Mandelkow E. Phosphorylation of Ser262 strongly reduces binding of tau to microtubules. Neuron 1993; 11 : 153–63. [Google Scholar]
  7. Lovestone S, Reynolds CH. The phosphorylation of tau : a critical stage in neurodevelopment and neurodegenerative processes. Neuroscience 1997; 78 : 309–24. [Google Scholar]
  8. Trojanowski JQ, Lee VMY. Phosphorylation of paired helical filament tau in Alzheimer’s disease neurofibrillary lesions: focusing on phosphatases. FASEB J 1995; 9 : 1570–6. [Google Scholar]
  9. Buée L, Bussière T, Buée-Scherrer V, Delacourte A, Hof PR. Tau protein iso-forms, phosphorylation and role in neurodegenerative disorders. Brain Res Rev 2000; 33 : 95–130. [Google Scholar]
  10. Sergeant N, David J P, Goedert M, et al. Two-dimensional characterization of paired helical filament-tau from Alzheimer’s disease. J Neurochem 1997; 69 : 834–44. [Google Scholar]
  11. Buée-Scherrer V, Buée L, Leveugle B, et al. Pathological tau proteins in postencephalitic parkinsonism : comparison with Alzheimer’s disease and neurodegenerative disorders. Ann Neurol 1997; 42 : 356–9. [Google Scholar]
  12. Buée-Scherrer V, Buée L, Hof PR, et al. Neurofibrillary degenera-tion in amyotrophic lateral sclerosis/ parkinsonismdementia complex of Guam. Immunochemical characte-rization of tau proteins. Am J Pathol 1995; 146 : 924–32. [Google Scholar]
  13. Buée-Scherrer V, Hof PR, Buée L, et al. Hyperphosphorylated tau proteins differentiate corticobasal degeneration and Pick’s disease. Acta Neuropathol 1996; 91 : 351–9. [Google Scholar]
  14. Sergeant N, Wattez A, Delacourte A. Neurofibrillary degeneration in progressive supranuclear palsy and corticobasal degeneration: tau pathologies with exclusely « exon 10 » isoforms. J Neurochem 1999; 72 : 1243–9. [Google Scholar]
  15. Mailliot C, Sergeant N, Bussière T, Caillet-Boudin ML, Delacourte A, Buée L. Phosphorylation of specific sets of tau isoforms reflects different neurofibrillary degeneration processes. FEBS Lett 1998; 433 : 201–4. [Google Scholar]
  16. Delacourte A, Sergeant N, Wattez A, Gauvreau D, Robitaille Y. Vulnerable neuronal subsets in Alzheimer’s disease and Pick’s disease are distinguished by their tau iso-form distribution and phosphorylation. Ann Neurol 1998; 43 : 193–204. [Google Scholar]
  17. Sergeant N, David JP, Lefranc D, Vermersch P, Wattez A, Delacourte A. Different distribution of phosphorylated tau protein isoforms in Alzheimer’s and Pick’s diseases. FEBS Lett 1997; 412 : 578–82. [Google Scholar]
  18. Sergeant N, Sablonnière B, Schraen-Maschke S, et al. Dysregulation of human brain microtubule-associated tau mRNA maturation in myotonic dystrophy type 1. Hum Mol Genet 2001; 10 : 2143–55. [Google Scholar]
  19. Zhukareva V, Vogelsberg-Ragaglia V, Van Deerlim V, et al. Loss of brain tau defines novel sporadic and familial tauopathies with frontotemporal dementia. Ann Neurol 2001; 49 : 165–75. [Google Scholar]
  20. Iseki E, Matsumura T, Marui W, et al. Familial frontotemporal dementia and parkinsonism with a novel mutation N296H mutation in exon 10 of the tau gene and a widespread tau accumulation in the glial cells. Acta Neuropathol 2001; 102 : 285–92. [Google Scholar]
  21. Neumann M, Schultz-Schaeffer W, Crowther RA, et al. Pick’s disease associated with the novel Tau gene mutation K369I. Ann Neurol 2001; 50 : 503–13. [Google Scholar]
  22. Pastor P, Pastor E, Carnero C, et al. Familial atypical progressive supranuclear palsy associated with homozigosity for the delN296 mutation in the tau gene. Ann Neurol 2001; 49 : 263–7. [Google Scholar]
  23. Delobel P, Flament S, Hamdane M, et al. Functional characterization of FTDP-17 tau gene mutations through their effects on Xenopus oocyte maturation. J Biol Chem 2002; 277 : 9199–205. [Google Scholar]
  24. Russ C, Powell JF, Zhao J, et al. The microtubule associated protein Tau gene and Alzheimer’s disease - an association study and meta-analysis. Neurosci Lett 2001; 314 : 92–6. [Google Scholar]
  25. Götz J, Probst A, Spillantini MG, et al. Somatodendritic localization and hyperphosphorylation of tau protein in transgenic mice expressing the longest human brain tau isoform. EMBO J 1995; 14 : 1304–13. [Google Scholar]
  26. Brion JP, Tremp G, Octave JN. Transgenic expression of the shortest human tau affects its compartmentalization and its phosphorylation as in the pretangle stage of Alzheimer’s disease. Am J Pathol 1999; 154 : 255–70. [Google Scholar]
  27. Götz J. Tau and transgenic animal models. Brain Res Rev 2001; 35 : 266–86. [Google Scholar]
  28. Lewis J, McGowan E, Rockwood J, et al. Neurofibrillary tangles, amyotrophy and progressive motor disturbance in mice expressing mutant (P301L) tau protein. Nat Genet 2000; 25 : 402–5. [Google Scholar]
  29. Braak H, Braak E. Neuropathological stageing of Alzheimer-related changes. Acta Neuropathol 1991; 82 : 239–59. [Google Scholar]
  30. Fewster PH, Griffin-Brooks S, MacGregor J, Ojalvo-Rose E, Ball MJ. A topographical pathway by which histopathological lesions disseminate through the brain of patients with Alzheimer’s disease. Dementia 1991; 2 : 121–32. [Google Scholar]
  31. Duyckaerts C, Colle MA, Dessi F, Grignon Y, Piette F, Hauw JJ. The progression of the lesions in Alzheimer disease: insights from a prospective clinicopathological study. J Neural Transm 1998; 53 (suppl) : 119–26. [Google Scholar]
  32. Delacourte A, Buée L, David JP, et al. Lack of continuum between cerebral aging and Alzheimer’s disease as revealed by PHF-tau and Aβ biochemistry. Alzh Rep 1998; 1 : 101–10. [Google Scholar]
  33. Delacourte A, David JP, Sergeant N, et al. The biochemical pathway of neurofibrillary degeneration in aging and Alzheimer’s disease. Neurology 1999; 52 : 1158–65. [Google Scholar]
  34. Delacourte A. The biochemical pathway of neurofibrillary degeneration in aging and Alzheimer’s disease. Neurology 2000; 54 : 538. [Google Scholar]
  35. Delacourte A, Sergeant N, Champain D, et al. The biochemical spreading of Tau and amyloid β precursor protein pathologies in aging and sporadic Alzheimer’s disease. Brain Aging 2001; 1 : 33–42. [Google Scholar]
  36. Lewis J, Dickson DW, Lin WL, et al. Enhanced neurofibrillary degeneration in transgenic mice expressing mutant tau and APP. Science 2001; 293 : 1487–91. [Google Scholar]
  37. Götz J, Chen F, Van Dorpe J, Nitsch RM. Formation of neurofibrillary tangles in P301l tau transgenic mice induced by Abeta 42 fibrils. Science 2001; 293 : 1491–5. [Google Scholar]
  38. Sergeant N, David JP, Champain D, et al. Progressive decrease of amyloid precursor protein carboxy-terminal fragments (APP-CTFs), associated with tau pathology stages, in Alzheimer’s disease. J Neurochem 2002; 81 : 663–72. [Google Scholar]

Les statistiques affichées correspondent au cumul d'une part des vues des résumés de l'article et d'autre part des vues et téléchargements de l'article plein-texte (PDF, Full-HTML, ePub... selon les formats disponibles) sur la platefome Vision4Press.

Les statistiques sont disponibles avec un délai de 48 à 96 heures et sont mises à jour quotidiennement en semaine.

Le chargement des statistiques peut être long.