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.

Tuesday, September 1, 2026

New research explores the earliest stages of coronary plaque inflammation

 Didn't your competent? doctor show you this video on how plaque forms and why cholesterol is not the problem?; INFLAMMATION IS! NO! So you DON'T have a functioning stroke doctor, do you? Why hasn't s/he been fired yet?

4 min. 36 seconds of explanation. This is what happened to my right carotid artery. My doctor should have explained this but no, he didn't say anything.

The accent is a bit hard to understand and needs to be  rerecorded to a laypersons understanding. 

New research explores the earliest stages of coronary plaque inflammation

A Cedars-Sinai Health Sciences University-led study has identified molecular changes that appear to trigger atherosclerosis years before inflammation, sharing their findings in European Heart Journal.[1]

The group believes this could a key discovery in the development of next-generation early prevention therapies. 

The study's authors found previously unrecognized molecular pathways and a possible master regulator protein called MLXIPL that could become future targets for clinicians working to stop plaque from ever developing.

“We analyzed proteins and gene activity in coronary artery tissue from young adults who died of trauma and had no known coronary artery disease, and we found that more than half already had preclinical atherosclerosis,” first author Sarah Parker, PhD, an associate professor of cardiology and biomedical sciences and co-director of the proteomics and metabolomics core at Cedars-Sinai Health Sciences University, said in a statement. “This suggests that changes in cellular metabolism and communication begin before the inflammation long considered a hallmark of the disease.”

Parker said this research provides a direct picture of what is happening inside the artery wall and may explain why some people are more vulnerable to heart disease than others.There have been studies showing very early atheroma lesions appearing in the first decade of life. Even with that in mind, however, questions have remained. 

"What we haven’t understood is what causes those early changes to progress into dangerous plaques that lead to heart attacks," Parker explained. "In studying coronary artery tissue before people ever developed symptoms, we were able to capture some of the earliest molecular changes that appear to set the disease in motion."

She said a big surprise from this research is that there are cellular metabolism and communication changes before the development of the classic inflammatory signals usually associated with atherosclerosis. There has been a lot of research focused on addressing inflammation to prevent heart disease, but this takes things even further and may offer help identify new preventive therapies.

"What our study suggests is that important molecular changes begin much earlier," Parker said. "If we want to prevent plaque from forming, we need to understand those earliest changes—not just what happens after inflammation has already taken hold."

She explained that proteins can tell researchers how the body’s cells are responding to risk factors like cholesterol, blood pressure or smoking. The differences in protiens found in people's cells can help explain why people with identical cholesterol levels will result in one never having coronary disease, while the other develops plaques.


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