| dc.description.abstract | Several studies have suggested that estrogen replacement therapy in postmenopausal women improves cognition and delay the onset of dementia associates with neurodegenerative diseases, as Alzheimer Disease (AD) or Parkinson. In addition, estrogens attenuate the effect of the injury for heart attack or cerebral traumatism, and exert influence on the mood. However, the mechanism whereby estrogens exert this neuroprotective effect is now unclear.
In this study, we propose two systems of cyclins (cyclin dependent kinase 5/protein 35-25 and cyclin dependent kinase 2/cyclin A) whose participation out of the cellular cycle and in association with the ovarian hormones can be involved in the mechanism of estrogen neuroprotection. This hypothesis comes from previous studies where have shown that such complexes participate in the activity of progesterone receptors and phosphorylation of Tau protein, this latter protein has an important role on the development of AD.
We used ovariectomized rats which were divided into treatment groups with different doses of 17β estradiol or progesterone, these treatments were administered during 2 weeks and then we analyze the cognitive abilities of the rats through autoshaping test. Finally, we analyzed the content of proteins of interest in the basal forebrain by western blot assay.
Our results suggest that improve of memory of ovariectomized rats is dose hormone dependent and it is related with changes in the complex of proteins studied. | |
