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.

Wednesday, August 14, 2019

Calcium is key to age-related memory loss

So YOU need to get your doctors and hospital to get research going in humans that will measure those calcium levels and provide ways to adjust those levels. If YOU don't do this your doctor and stroke hospital will do nothing. 

Calcium is key to age-related memory loss

Credit: CC0 Public Domain
Research at the University of Leicester is offering new clues into how and why cognitive functions such as memory and learning become impaired with age. A paper published recently in a specialist neuroscience journal shows that a crucial factor is calcium levels in specific cells in the brain.
As we get older, our memory starts to fail and it becomes harder to learn new things. It would not be unreasonable to assume that this is caused by gradually dying off but that doesn't happen. So what causes age-related cognitive impairment?
The answer lies in synapses, the electro-chemical connections between neurons that use neurotransmitter molecules to create the web of functions within the central nervous system. Professor Nick Hartell from the University of Leicester's Department of Neuroscience, Psychology and Behaviour looked at whether calcium levels in the hippocampus, part of the brain necessary for learning and memory, might play a part.
Most research in this area has concentrated on post-synaptic cells—the ones which receive neurotransmitters—simply because measuring calcium levels in pre-synaptic cells is very difficult. Nick and his colleagues stepped up to the challenge, by developing a special strain of mice which express a calcium-sensing within the pre-synaptic parts of their hippocampus.
The research used mazes and object recognition tests to study the cognitive functions of mice at ages of 6, 12, 18 and 24 months, and found a clear correlation between cognitive ability and pre-synaptic . In older mice, which perform less well in the tests, the homeostatic processes that should keep intracellular calcium within limits start to falter, creating a build-up of calcium in pre-synaptic cells within the hippocampus.
Experimentally raising the level of intracellular pre-synaptic calcium in the brains of young mice altered the synaptic properties so that they behaved like those from the older mice. Most fascinating of all the results is that the reverse is also true: lowering intracellular in old mouse brains rejuvenates their synapses—which obviously has enormous potential significance for age-related health issues in humans.

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