Alzheimer disease models and human neuropathology: similarities and differences

Animal models aim to replicate the symptoms, the lesions or the cause(s) of Alzheimer disease. Numerous mouse transgenic lines have now succeeded in partially reproducing its lesions: the extracellular deposits of Aβ peptide and the intracellular accumulation of tau protein. Mutated human APP transgenes result in the deposition of Aβ peptide, similar but not identical to the Aβ peptide of human senile plaque. Amyloid angiopathy is common. Besides the deposition of Aβ, axon dystrophy and alteration of dendrites have been observed. All of the mutations cause an increase in Aβ 42 levels, except for the Arctic mutation, which alters the Aβ sequence itself. Overexpressing wild-type APP alone (as in the murine models of human trisomy 21) causes no Aβ deposition in most mouse lines. Doubly (APP × mutated PS1) transgenic mice develop the lesions earlier. Transgenic mice in which BACE1 has been knocked out or overexpressed have been produced, as well as lines with altered expression of neprilysin, the main degrading enzyme of Aβ. The APP transgenic mice have raised new questions concerning the mechanisms of neuronal loss, the accumulation of Aβ in the cell body of the neurons, inflammation and gliosis, and the dendritic alterations. They have allowed some insight to be gained into the kinetics of the changes. The connection between the symptoms, the lesions and the increase in Aβ oligomers has been found to be difficult to unravel. Neurofibrillary tangles are only found in mouse lines that overexpress mutated tau or human tau on a murine tau −/− background. A triply transgenic model (mutated APP, PS1 and tau) recapitulates the alterations seen in AD but its physiological relevance may be discussed. A number of modulators of Aβ or of tau accumulation have been tested. A transgenic model may be analyzed at three levels at least (symptoms, lesions, cause of the disease), and a reading key is proposed to summarize this analysis

The fomes annosus

Cet article est une revue de la bibliographie existante sur le Fomes annosus et tente de faire le point sur les connaissances actuelles sur ce sujet. 51 références bibliographiques sont citées qui ne représentent qu'une faible proportion des documents disponibles sur la question. L'auteur décrit le champignon dans les différentes phases de sa biologie et dans un paragraphe particulier, il fait état des méthodes de lutte actuellement connues ainsi que celles, non encore au point, qui font l'objet de recherches.This article is a survey of the existing bibliography on the Fomes annosus and furthermore, it endeavous to determine the extent of the knowledge presently at hand on the subject. 51 works of bibliographical référence are mentioned ; they represent only a small proportion of the available total documents on the question. The writer describes the mushroom in its various biological stages. He notes in a special paragraph the methods of prevention known at present, as well as those that are still to be perfected and which make now the object of scientific research