It appears that the key to cell survival in these hypoxic
conditions is the production of a protein called hamartin. Hamartin, or Tsc1, is a protein produced by
hippocampus cells in the brain when they lack oxygen. Hamartin appears to cause the cells to stop producing other
proteins and instead break-down those it already has, thus temporarily halting its use of oxygen. In the study, researchers were able to isolate the gene that regulates hamartin expression in rats, and turn it off. This caused a 38% increase in the rate of cell death in stroke in the animals, compared to those with an active hamartin gene, indicating the protective role that harmartin plays.
The goal of the researchers is to be able to find a way to
turn on the genes to produce hamartin in other brain cells. The BBC article suggests that an additional, long-term
goal is to produce a drug that could be given to a patient in the early stages
of stroke, in order to cause their own cells to produce enough hamartin to allow
them to survive. Of course, this is highly reliant on the ability of stroke to be detected in its early stages; administration of hemartin significantly after the onset of stroke would have negligible benefits. It should additionally be noted though that other experts contacted by the journalist indicate that this may be a long way off. Nevertheless, the prospect is certainly an exciting one.
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ReplyDeleteThis particular post caught my attention because I am try to regularly read the science stories from BBC when I read their site for daily news! I thought it was interesting that you posted about a different protein that potentially acts as an alleviation/treatment to ischemic strokes other than the leukocytes and cytokines that are commonly brought up with this topic (T-cell, B-cell, etc.)
ReplyDeleteI like that the authors of this paper explained their study of hamartin (TSC1) as a neuroprotective agent under two limited domains: (1)the resistance of CA3 hippocampal neurons to global ischemia and (2) the tolerance conferred by ischemic preconditioning (IPC). I found this significant because it covers both a synthetically induced form of stroke as seen in almost all conducted research involving ischemic brain injury as well as acquired stroke seen in human stroke patients.
I was wondering if you thought that this type of treatment of stroke has potential to become a regularly used technique in opposition to T-cell/B-cell suppression and other reperfusion therapy techniques? Do you think that the 38% increase seen when turning off hemartin is significant enough to realistically utilize it as a thrombolytic therapy or percutaneous coronary invervention?
Good post though by the way...I like the title!
I'm optimistic that with more research this may become a viable treatment technique. I think that a major area for further research would be the effect of hamartin on CA1 cells. Since these have more plasticity than those CA3 cells found in the hippocampus, our ability to save them may allow for a faster recovery from a stroke.
ReplyDeleteAs far as whether or not 38% is a high enough percentage to warrant its use, I'll again say that more research should be done, first to confirm this value, and then to see what therapeutic role it could play. Perhaps treatments should not be done that only utilize hamartin, but in conjunction with T/B-cell suppression, it may be a worthwhile avenue of treatment.
I found this article on hamartin and stroke intriguing. I agree with Daniel that with more research hamartin might be a great target in the treatment of stroke. The post mentions that the goal of a potential drug would be to turn on genes that stimulate the production of hamartin in brain cells. The idea would be to start treatment before stroke occurs, and that this treatment would help brain cell survival during a stroke. Of course it is hard to predict when stroke might occur. To address that issue it might be important to evaluate the health of individuals, and see what their risks are of developing a stroke during a check up. If this drug was started and no stroke occurred, would their be any consequence to an increased concentration of hamartin in the brain? It's hard to say whether this treatment would actually be viable. However, it appears to be a very good area of research, and might help provide protection to future stroke victims.
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