|
Olfactory aging in normal mice and in an Alzheimer’s disease model: implications of neurogenesis and noradrenergic system| old_uid | 9338 |
|---|
| title | Olfactory aging in normal mice and in an Alzheimer’s disease model: implications of neurogenesis and noradrenergic system |
|---|
| start_date | 2010/12/01 |
|---|
| schedule | 14h-18h |
|---|
| online | no |
|---|
| details | la soutenance sera en anglais |
|---|
| summary | Olfactory deficits are present during normal aging and Alzheimer’s disease. These deficits occur very early in Alzheimer’s disease and could be among the first signs of the disease. Thus, the definition and comparison of olfactory deficits appearing in normal aging versus Alzheimer’s disease and their cellular correlates, including changes in neurogenesis and noradrenergic system, both involved in olfactory perception and affected in Alzheimer’s disease, are crucial for better understanding of the disease. Our first study was aimed at characterizing olfactory function and it’s plasticity in normal aging in mice. This work provides new data regarding aging of perception and sets up the background for comparing olfactory deficits in normal and pathological aging. Our second study confirms that olfactory deficits occurs early in APP/PS1 mice, an Alzheimer’s disease model, and confirms the implication of noradrenergic depletion the pathology. Indeed, a chronic DSP4-induced depletion in noradrenalin aggravates amyloïd deposition and olfactory deficits. Taken together, these data provide a strong support to the use of the olfactory modality to study aging of perception and to the implication of noradrenergic depletion in both cognitive and histo-pathological early signs of the disease. |
|---|
| responsibles | Gervais |
|---|
| |
|