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 2, 2023

Decoding Cognitive Decline: Key Aging Mechanism Discovered

 So you found something, but did nothing to make it useful to patients.

Decoding Cognitive Decline: Key Aging Mechanism Discovered

Summary: Researchers have identified the key mechanism that may be responsible for the cognitive decline observed in the natural aging process. They found that the mis-regulation of a brain protein known as CaMKII, vital for memory and learning, is linked to this decline.

Aging decreases S-nitrosylation, a process modifying specific brain proteins, including CaMKII, thereby impairing memory and learning ability. The findings point towards potential pharmacological strategies to normalize protein nitrosylation, potentially combating age-related cognitive decline.

Key Facts:

  1. Researchers have found that the mis-regulation of a brain protein called CaMKII could be the central mechanism behind cognitive decline related to normal aging.
  2. The study revealed that normal aging reduces the process of S-nitrosylation, modifying specific brain proteins, which impairs memory and learning ability.
  3. These findings open potential avenues to develop drugs or other therapeutic interventions that can normalize the nitrosylation of CaMKII, possibly staving off normal cognitive decline.

Source: University of Colorado

Scientists at the University of Colorado Anschutz Medical Campus have discovered what they believe to be the central mechanism behind cognitive decline associated with normal aging.

“The mechanism involves the mis-regulation of a brain protein known as CaMKII which is crucial for memory and learning,” said the study’s co-senior author Ulli Bayer, PhD, professor of pharmacology at the University of Colorado School of Medicine. “This study directly suggests specific pharmacological treatment strategies.”

The study was published today in the journal `Science Signaling.’

Researchers using mouse models found that altering the CaMKII brain protein caused similar cognitive effects as those that happen through normal aging.

Bayer said that aging in mice and humans both decrease a process known as S-nitrosylation, the modification of a specific brain proteins including CaMKII.

“The current study now shows a decrease in this modification of CaMKII is sufficient to cause impairments in synaptic plasticity and in memory that are similar in aging,” Bayer said.

Normal aging reduces the amount of nitric oxide in the body. That in turn reduces nitrosylation which reduces memory and learning ability, the study said.

Bayer said the new research opens the way toward developing drugs and other therapeutic interventions that could normalize the nitrosylation of the protein. He said that holds out the possibility of treating or staving off normal cognitive decline for an unknown period of time.

He pointed out that this would only work in normal age-related cognitive decline, not the decline seen in Alzheimer’s disease and dementia.

“We know this protein can be targeted,” Bayer said.  “And we think it could be done pharmacologically. That is the next logical step.”

About this aging and cognition research news

Author: David Kelly
Source: University of Colorado
Contact: David Kelly – University of Colorado
Image: The image is credited to Neuroscience News

Original Research: Closed access.
Decreased nitrosylation of CaMKII causes aging-associated impairments in memory and synaptic plasticity in mice” by Ulli Bayer et al. Science Signaling

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