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, January 8, 2020

Elevating acetyl-CoA levels reduces aspects of brain aging

Is your doctor and stroke hospital looking at this and IMMEDIATELY realizing this might be a solution to your 5 lost cognitive years from your stroke. 

Or is your doctor and stroke hospital doing nothing with this? Do you prefer your incompetence NOT KNOWING? OR NOT DOING?

Their reasons for doing nothing?

Laziness? Incompetence? Or just don't care? No leadership? No strategy? Not my job?

 

Elevating acetyl-CoA levels reduces aspects of brain aging



  1. Antonio Currais  Is a corresponding author
  2. Ling Huang
  3. Joshua Goldberg
  4. Michael Petrascheck
  5. Gamze Ates
  6. António Pinto-Duarte
  7. Maxim N Shokhirev
  8. David Schubert
  9. Pamela Maher  Is a corresponding author
  1. The Salk Institute for Biological Studies, United States
  2. The Scripps Research Institute, United States
Research Article
Cite
as: eLife 2019;8:e47866 doi: 10.7554/eLife.47866


Abstract

Because old age is the greatest risk factor for dementia, a successful therapy will require an understanding of the physiological changes that occur in the brain with aging. Here, two structurally distinct Alzheimer's disease (AD) drug candidates, CMS121 and J147, were used to identify a unique molecular pathway that is shared between the aging brain and AD. CMS121 and J147 reduced cognitive decline as well as metabolic and transcriptional markers of aging in the brain when administered to rapidly aging SAMP8 mice. Both compounds preserved mitochondrial homeostasis by regulating acetyl-coenzyme A (acetyl-CoA) metabolism. CMS121 and J147 increased the levels of acetyl-CoA in cell culture and mice via the inhibition of acetyl-CoA carboxylase 1 (ACC1), resulting in neuroprotection and increased acetylation of histone H3K9 in SAMP8 mice, a site linked to memory enhancement. These data show that targeting specific metabolic aspects of the aging brain could result in treatments for dementia.
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