Deans' stroke musings: Epigenetics and stroke risk

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.

Friday, October 19, 2012

Epigenetics and stroke risk – beyond the static DNA code

You'll have to ask your doctor to decipher this 18 page article. They need to be up on epigenetics anyway. Remember to specify that not knowing this information is stressful and may shrink your brain.

http://scholar.google.com/scholar_url?hl=en&q=http://www.dovepress.com/getfile.php%3FfileID%3D14237&sa=X&scisig=AAGBfm2WeXvWA9bM6WtyEKweh7Zg_M0V-Q&oi=scholaralrt
Abstract: Advances in high-throughput genome sequencing and genome-wide association studies indicate that only a fraction of estimated variability in stroke risk can be explained by genetic variation in protein-coding genes alone. Epigenetics is defined as chromatin-based mechanisms important in the regulation of gene expression that do not involve changes in the DNA sequence per se. Epigenetics represents an alternative explanation for how traditional risk factors confer increased stroke risk, provide a newer paradigm to explain heritability not explained by genetic variation, and provide insight into the link between how the environment of a cell can interact with the static DNA code. The nuclear-based mechanisms that contribute to epigenetic gene regulation can be separated into three distinct but highly interrelated processes: DNA methylation and hydroxymethylation; histone density and posttranslational modifications; and RNA-based mechanisms. Together, they offer a newer perspective on transcriptional control paradigms in blood vessels and provide a molecular basis for understanding how the environment impacts the genome to modify stroke susceptibility. This alternative view for transcriptional regulation allows a reassessment of the cis/trans model and even helps explain some of the limitations of current approaches to genetic-based screens. For instance, how does the environment exert chronic effects on gene expression in blood vessels after weeks or years? When a vascular cell divides, how is this information transmitted to daughter cells? This review provides an introduction to epigenetic concepts and a conceptual framework for understanding the shortcomings of an approach to stroke research that focuses solely on the static DNA code. Additionally, it will discuss classical and emerging mechanisms of epigenetic gene regulation that are especially relevant to large-vessel ischemic stroke.