par Brion, Jean Pierre 
Référence Bulletin et mémoires de l'Académie royale de médecine de Belgique, 147, 11-12, page (481-9; discussion 490-1)
Publication Publié, 1992
Référence Bulletin et mémoires de l'Académie royale de médecine de Belgique, 147, 11-12, page (481-9; discussion 490-1)
Publication Publié, 1992
Article révisé par les pairs
| Résumé : | Neurofibrillary tangles and senile plaques are the characteristic neuropathological lesions of Alzheimer's disease. Neurofibrillary tangles are composed of a microtubule-associated protein, the tau protein. This protein plays a role in the development of neuronal polarity and the stabilisation of microtubules. In Alzheimer's disease, tau proteins are abnormally phosphorylated on several sites. This abnormal phosphorylation might induce the modifications of the microtubule network observed in affected neurones. The main component of the senile plaque is an amyloid deposit made of a polypeptide (beta/A4 amyloid) which derives from a larger precursor. The overexpression of this precursor in experimental models or mutations of its gene leads to the development of neuropathological lesions. The relationships between cytoskeletal abnormalities and beta/A4 amyloid are further discussed. |
