| title: | Mitochondrial component of the neuroprotective action of dehydroepiandrosterone |
|---|---|
| reg no: | ETF5219 |
| project type: | Estonian Science Foundation research grant |
| subject: |
1.9. Genetics, Physiology and Microbiology 3. Medical Sciences |
| status: | completed |
| institution: | University of Tartu |
| head of project: | Allen Kaasik |
| duration: | 01.01.2002 - 31.12.2004 |
| description: | Dehydroepiandrosterone (DHEA) and its sulphated derivative DHEAS are the most abundant circulating steroids in humans. Its concentration sharply drops after birth and starts to rise few years before puberty with peak levels obtained in the third decade of life. Thereafter, a marked continuos decline in DHEA(S) secretion is observed with elderly subjects secreting only 20% compared to young subjects. As this decline might be related to some impairment of health, also at the level of CNS, people considering compensatory administration of DHEA beneficial. The commercial availability of DHEA outside the regular pharmaceutical network in States and also in some countries in Europe, including Estonia, have lead to improper use of that compound in the absence of any medical indication. As a result, the scientific community is currently under the pressure of growing number of request from elderly individuals to find an answer to number of physiological and medical points. What is the physiological role of DHEA? How does the deficit of this natural compound during ageing compromises the health and whether there it has merit being compensated? Are there side effects? For that reasons the main aims of current project are to find out 1) what is the mechanism of neuroprotective action of dehydroepiandrosterone, 2) whether the another steroids having similar mechanism of action could be used as a neuroprotectants and 3)what is the mechanism of the toxicity of dehydroepiandrosterone at pharmacological concentrations. The scientific impact of the current project is 3-fold. First, it could provide a plausible explanation for the mechanism of the neuroprotective effect of that important neurosteroid DHEA. Second, it could provide a plausible explanation for the cytotoxic effect of DHEA at pharmacological concentrations occurring during DHEA replacement therapy that has its clinical impact (patients with cytochrome c oxidase deficiency). And third it may lead to discovery of new uniporter inhibitors which clearly have a real therapeutic potential. All together this information, when obtained, allows to create a qualitatively new and objective concept about the biological role dehydroepiandrosterone. |
| project group | ||||
|---|---|---|---|---|
| no | name | institution | position | |
| 1. | Allen Kaasik | University of Tartu Medical Faculty Dept Pharmacology | sen researcher | |
| 2. | Anti Kalda | Univ Tartu | sen researcher | |
| 3. | Aleksander Žarkovski | Univ Tartu | prof | |