Amphithéâtre Marguerite de Navarre, Site Marcelin Berthelot
Open to all
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For this last lecture of the year, I'm going to take up a bit on telomeres, the end of the lecture from two weeks ago and then bring everything that was discussed back to memory in order to open up a bit more widely on the integration of the various mechanisms of aging and prepare you for the rest of the lecture, in 2014. I'll start by reminding you of the grain and periglomerular neuron renewal pattern of the olfactory bulb (DIA VI.2). I'll also briefly remind you that aging is accompanied by a decline in the renewal of these cells, accompanied by a parallel decline in telomerase activity (DIA VI.3).

Last week, we began discussing the possible link between telomere shortening and morphological changes in neurons (and not just their senescence and apoptosis). This is important because it suggests another - possibly physiological - function of telomeres. As I had pointed out, it turns out that laboratory mice have much longer telomeres than humans and wild-type mice (40 to 60 kbp versus 5 to 10 kbp). This is why, as you saw last week, analyses are carried out on the3rd,4th or5th generation (G3, G4 or G5) of mice lacking telomerase activity (mutation of Terc, the RNA substrate of telomerase).