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Neuroprotection induced by the adenosine A1-receptor and IL-6: Do they use the same mechanisms?

Bourgonje, A.M. (2009) Neuroprotection induced by the adenosine A1-receptor and IL-6: Do they use the same mechanisms? Bachelor's Thesis, Biology.

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In many chronic neurodegenerative diseases, as well as in acute conditions, there is excess of glutamate which results in a toxic environment for neurons. This toxicity is responsible for the neuronal cell death found in these diseases. Substances like adenosine and Interleukin-6 (IL-6) have been shown to induce protection against this glutamate toxicity. Adenosine exerts this neuroprotective effect via the adenosine A1-receptor. However the mechanisms by which IL-6 induces this neuroprotection are still unclear. A connection between the two seemed likely because they were found in many of the same conditions. It has been shown that IL-6 is released from astrocytes by activation of the adenosine A2b-receptor. In other studies is has been shown that IL-6 upregulates the adenosine A1-receptor. It is also shown that without the upregulation of the A1-receptor by IL-6 the receptor has no neuroprotective properties via the A1-receptor. This could mean that the adenosine protection effect needs IL-6. These facts all support a link between adenosine and IL-6 neuroprotection. It could be that the neuroprotective properties assigned to IL-6 could all be due to it upregulating the adenosine A1-receptor. Also it could be that IL-6 uses the same mechanisms for its protection. Although the mechanisms by which IL-6 induces protection are not clear the release of IL-6 is not only dependent on adenosine. The P2Y1-receptor on the astrocyte can also release IL-6 when its ligand ATP binds to it. All this information could eventually be used in a treatment for the conditions glutamate toxicity causes neuronal death.

Item Type: Thesis (Bachelor's Thesis)
Degree programme: Biology
Thesis type: Bachelor's Thesis
Language: English
Date Deposited: 15 Feb 2018 07:28
Last Modified: 15 Feb 2018 07:28

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