par Brion, Jean Pierre 
Référence Bulletin et mémoires de l'Académie royale de médecine de Belgique, 154, 6 Pt 2, page (287-294)
Publication Publié, 1999
Référence Bulletin et mémoires de l'Académie royale de médecine de Belgique, 154, 6 Pt 2, page (287-294)
Publication Publié, 1999
Article révisé par les pairs
| Résumé : | Neurofibrillary tangles, a hallmark neuropathological lesion of Alzheimer's disease and of the other tauopathies, are composed of hyperphosphorylated tau proteins (a microtubule-associated protein) assembled in the form of abnormal filaments. Hyperphosphorylation of tau proteins appears to be an early phenomenom, preceding their aggregation into fibrillar structures. This hyperphosphorylation could result from changes in the activation of signalling cascades. Presenilins, and their mutations, could be responsible for these changes and, by their ability to interfere with APP metabolism, play a central role in the formation of both neurofibrillary tangles and A beta amyloid deposits. |
