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, January 10, 2016

Can An Anti-Asthma Drug Rejuvenate the Brain? montelukast

Your doctor should be vastly interested in how this can be applied to stroke survivors. But don't worry this will never be followed up on because we have NO stroke strategy or stroke leadership in any part of stroke and this will fall thru the cracks. Our fucking failures of stroke associations once again will lead the way to failure by not doing anything about this.

Can An Anti-Asthma Drug Rejuvenate the Brain?

A couple of paragraphs from there.

This group of researchers from Austria, Germany, Italy and Croatia presented a new therapy that, according to their own words, can “functionally rejuvenate the aged but otherwise healthy brain”. And the therapeutic agent is probably surprising: it’s an anti-asthmatic drug named montelukast.
The authors had previously identified a molecule involved in asthma pathology as being elevated in ageing, contributing to neuroinflammation and cognitive impairment. This led them to the hypothesis that other mechanisms originally related to peripheral inflammatory conditions such as asthma might affect the central nervous system, potentially contributing to degenerative processes.
Leukotrienes are a group of molecules that mediate inflammatory reactions associated with increased vascular permeability. Increased levels of leukotrienes have been reported in a number of neurological conditions, as well as in the aged brain. Although their role is mostly unclear, it is believed that they may mediate inflammatory responses in the brain and blood vessels. The drug they used, montelukast, acts by blocking leukotriene activity, being highly successful in asthma.
According to their data, montelukast seems to be able to reduce the levels of inflammatory molecules in the brain, restore the blood-brain barrier’s integrity and increase neurogenesis in the brain of aged rats. As a consequence, montelukast treatment also restores cognitive function in the old animals.
Montelukast seems to be able to cross the blood-brain barrier and it had previously been shown to have a protective effects in animal models of neurodegenerative diseases, including Huntintgon’s and Alzheimer’s disease, as well as in induced loss of memory function, spinal cord and brain injuries and stroke, decreasing cognitive and structural deficits.
Here, they showed that this anti-asthma drug can reduce age-associated changes, improving learning and memory in old rats, reducing the inflammation-induced activation of glial cells in the brain, and restoring neurogenesis in the hippocampus of old rats most likely by targeting leukotriene actions in the brain.

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