Deans' stroke musings: Roles of 5HT1A receptor in CNS neurogenesis and ADAM21 in spinal cord injury

Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 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:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. 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 lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Sunday, February 26, 2012

Roles of 5HT1A receptor in CNS neurogenesis and ADAM21 in spinal cord injury

Even if this is for spinal cord injury we need the knowledge gained by this.
http://gradworks.umi.com/34/89/3489325.html
Abstract:
These studies set out to identify strategies to rescue and repair the adult nervous system. First, we investigated the role of ciliary neurotrophic factor (CNTF) in 5HT1A receptor-induced neurogenesis in the rodent brain. Systemic treatment with an agonist, 8-OH-DPAT, increased neurogenesis only in rats and not mice, and only in one of the two neurogenic regions. This increase was not mediated by CNTF. These data suggest that translation of 5HT1A-based studies to human cell replacement therapies should be reconsidered. Secondly, the role of the plasticity-associated metalloprotease ADAM21 after spinal cord injury was investigated by comparing ADAM21-deficient mice to their wildtype littermates. No differences in behavioral or histology were found. However, a comprehensive metalloproteinase gene array revealed that ADAM21 regulates a cluster of inflammatory genes following injury. This leaves a potential for discovery of specific pharmaceutical ADAM21 inhibitors to reduce detrimental inflammatory processes following spinal cord injury.
full dissertation here: