My reply to this article was rejected.
article here:
http://www.irishhealth.com/article.html?id=16471
My reply, I thought it was damn good.
If you think about it you could get more for your money if you start researching hyperacute therapies that stop the cascade of neuronal death. Some have only been tested in mice and rats so needed are Phase II and III trials. Literally dozens of these possibilities. Every neurologist should be able to point to the studies I quoted from. Try
anti-depressants,KCC2,
"The death of neurons in the brain can be triggered by an imbalance of oxygen - known as oxidative damage, or where cells are incorrectly instructed to die by a neurotransmitter - a process known as excitotoxicity. KCC2 protects against both.
Mannan Binding Lectin-Associated Serine Protease-2 (MASP-2),
By binding with a molecule known as PAR polymer, Iduna prevents the movement of cell-death-inducing factor (AIF) into a cell’s nucleus.
It’s not just a delay of death, but real protection that lasts for about 72 hours.”
Iduna protects the brain from glutamate excitotoxicity and stroke by interfering with poly(ADP-ribose) polymer-induced cell death
Several years ago, scientists realized that the same enzyme that gives bats more blood for their bite may also help stroke victims by breaking down blood clots. Dubbed Draculin, this blood-clot-bashing drug has now entered a phase 2 study:
extends that window up to 9 hours
JNK,
tumeric,
One compound, called CNB-001, which was derived from curcumin,
Irish coffee injection(caffeinol),
The experimental drug, called caffeinol, has the potency of two cups of strong coffee and a small shot of alcohol. When injected into rats within three hours of an artificially stimulated stroke, brain damage was cut by up to 80 per cent.
xenon gas,
Earlier preclinical work by the team showed that xenon was effective as a neuroprotectant, stopping processes present during strokes or brain and spinal cord injuries that would damage nerve cells. They found that xenon was capable of blocking the effects of a particular type of glutamate receptor, the same receptor implicated in the pathway that leads to nerve cell death.
Sigma-1 receptors,
Professor Tadeusz Wieloch and his colleagues have found a way to activate a protein in the brain, the sigma-1 receptor, which plays an important role in the brain’s recovery during the critical period after the injury.
We then injected the rats with a specific substance that activated the sigma-1 receptor and found that the rats regained their function more quickly than the untreated animals”, explains Professor Wieloch.
Of course he doesn't say what the injected substance is but it has to be published somewhere.
Alpha-B-crystalline: this is the name of the substance, which reduces the inflammatory response. Naturally present in the lens of the eye (the transparent lens located behind the iris), this protein would significantly reduce the size of the consecutive stroke brain. 12 hours after the stroke.
alpha-B-crystallin, acts as a brake on the immune system, lowering levels of inflammatory molecules whose actions are responsible for substantial brain damage above and beyond that caused by the initial oxygen deprivation of a stroke.
When systemically administered 24 hours after stroke,perlecan, domain V,was well tolerated, reached infarct and peri-infarct brain vasculature, and restored stroke-affected motor function to baseline pre-stroke levels
the genetic activation of the nucleic acid protein Caspase-3 – a member of the cysteine-aspartic acid protease (caspase) family – is a major factor in loss of neuronal tissue and associated apoptosis (programmed cell death).
Carbon nanotubes (CNTs) have been used as a delivery vehicle
CNTs to deliver small interfering RNAs – nucleic acids which block gene expression – to stop production of this enzyme.
"The destiny of neurons in a damaged brain depends on a tiny equilibrium between pro-survival and pro-death signals. We wanted to know what KCC2 was signalling for - was it killing neurons or protecting them after an injury? Our study has found that KCC2 actually rescues the damaged cells."
But when they artificially increased the levels of KCC2 (by stimulating its expression using gene therapy), they found the damaged cells were protected from further damage, and death.
CDB3 peptide spares neurons from death following traumatic brain injury following stroke and accidents. injection within 2 hours.
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