Deans' stroke musings

Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:http://oc1dean.blogspot.com/2010/11/my-background-story_8.html

Wednesday, August 3, 2016

PET imaging of adult neurogenesis may contribute to better diagnosis of depression and evaluation of drug therapy effectiveness

Whenever we do get interventions that supposedly deliver neurogenesis we can use this to objectively verify that neurogenesis has actually occurred.  But I bet our neurogenesis researchers won't do that unless our great stroke association follows up with the researchers.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=166744&CultureCode=en
Scientists from the RIKEN Center for Life Science Technology (CLST) in Japan have used a new non-invasive PET scanning technique to obtain images of neuron proliferation in the subventricular zone and subgranular zone of the hippocampal dentate gyrus. Neurogenesis in the hippocampal dentate gyrus is known to be particularly affected by depression.
              These two areas are known to be neurogenic regions, where neural stem cells give rise to new neurons throughout our lives. Hippocampal neurogenesis is known to be associated with depression and the effect of antidepressive medication, but it is also involved in learning and memory, so scientists are keen to find techniques that can monitor cell proliferation in the region. However, the process of neurogenesis is very hard to monitor non-invasively. It is possible using magnetic resonance imaging, but with MRI the tracers do not move into the brain effectively and must be injected directly into the brain fluid, making is invasive and difficult to perform.
              Positron emission tomography (PET) is another method that has been used. Previously, attempts have been made to use a molecule called [18F]FLT as a marker for cell proliferation in the brain in PET, but unfortunately the difference in signal strength between regions with and without cell growth was small. “We were not exactly sure why this was happening,” says Tamura, “but surmised that it is because the body actively pumps the molecule out of the brain through the blood-brain barrier, using active transport mechanisms. This means that it is difficult for [18F]FLT to accumulate in the brain in sufficient concentrations to allow effective imaging.”
              To test whether this was the case, they tried injecting rats with a drug called probenecid, which is known to inhibit the active transport of molecules like [18F]FLT outside of the brain. They were happy to see that the strategy worked. They found clear signals of neurogenesis in the two areas of the adult brain, and these signals were significantly decreased in the hippocampal dentate gyrus of rats that had been treated with corticosterone to trigger depression. When the rats were treated with an anti-depressive selective serotonin reuptake inhibitor, the amount of cell proliferation was shown to increase, demonstrating that the drugs were countering the loss of neurogenesis caused by the corticosterone.
              According to Yosky Kataoka, who led the research team, “This is a very interesting finding, because it has been a longtime dream to find a non-invasive test that can give objective evidence of depression and simultaneously show whether drugs are working in a given patient. We have shown that it is possible, at least in experimental animals, to use PET to show the presence of depression and the effectiveness of drugs. Since it is known that these same brain regions are involved in depression in the human brain, we would like to try this technique in the clinic and see whether it turns out to be effective in humans as well.”

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