Stroke recovery: it’s in the genes

 Doesn't make a damn bit of difference; Survivors still expect 100% recovery!

Stroke recovery: it’s in the genes

UCLA Health researchers say genetic variants were strongly associated with depression, PTSD and cognitive health outcomes

24-Jul-2024 2:05 PM EDT, by University of California, Los Angeles (UCLA), Health Sciences contact patient services

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New research led by UCLA Health has found that specific genes may be related to the trajectory of recovery for stroke survivors, providing doctors insights useful for developing targeted therapies. 

Published in the journal Stroke this month, the findings were part of an exploratory study that sought to find if candidate genes could predict a higher likelihood of stroke outcomes related to depression, post-traumatic stress disorder and cognitive decline.  

Dr. Steven C. Cramer, MD, the study’s lead author and a professor of neurology at UCLA, said while there are some predictors physicians can use to anticipate stroke recovery, such as a patient’s age or baseline health, they only tell part of the story. 

“In the big picture, the issue that we face is that, when somebody has a stroke, it’s hard to anticipate what's going to come next,” said Cramer. “People look up to us from the gurney in the ER and say, ‘What's next? What's going to happen to me?’ People want to understand what their trajectory will be, people want to have a sense of how well going to be, or not, and what treatments are available to them.”  

Similarly, clinicians who treat patients with stroke need improved methods to understand how a patient will fare in order to develop a personalized medicine approach for each individual, Cramer said. 

Past studies have provided evidence that genetic differences are related the process of stroke recovery, but there has been limited study on the specific outcomes with which these genes are associated. For example, most previous genetic studies related to stroke have relied on the modified Rankin scale, which is a measure of global disability that combines recovery data across all behaviors into one single-digit score. 

However, Cramer said this scoring system does not account for the granular differences in stroke outcomes for patients, such as a patient having improved movement but continued severe depression, or having persistent anxiety but showing good recovering of arm movement. As a result, Dr. Cramer, in collaboration with Dr. E. Alison Holman at UC Irvine, sought to determine whether there was a method to more precisely measure the various behavioral outcomes among stroke survivors. 

To do this, Cramer and his team measured details for a group of candidate genes to examine in more than 700 patients enrolled throughout the U.S. Additionally, researchers conducted detailed behavioral assessments of the participants’ cognitive health, depression, post-traumatic stress disorder symptoms, and other deficits for one year after the stroke.  

The study found significant associations between certain genes and these behavioral health outcomes. Specifically, the rs6265 gene variant was associated with poorer cognition. This gene variant is related to brain-derived neurotrophic factor, or BDNF, which is the most common growth factor in the brain and is strongly associated with learning. About 20-30% of people are estimated to have this genetic variant, which slows the release of BDNF. 

“Your brain gushes out BDNF when you’re learning new things,” “Hopefully your brain is gushing out BDNF at this very moment. People who have this gene variant had poorer cognitive status at one year.” 

Environmental factors, such as stressors, also played a role in genetic expression among stroke patients. Patients with the gene variants rs4291 and rs324420 were at higher risk for developing more severe depression and PTSD symptoms after one-year post-stroke. 

“The more stress they reported, the more the gene variant was associated with poorer outcomes,” Cramer said. 

Another variant, rs4680, was linked to lower depression and PTSD symptoms. 

While the results still require independent verification, Cramer said these insights could help physicians and other allied health professionals tailor treatment options for patients based on a simple genetic test. 

“If these discoveries are validated as accurate, you could look at someone on the day they have their stroke and say, ‘I know that on average you are at higher risk of a poorer outcome regarding cognitive function a year from now,’” Cramer said. “Maybe those are the people that need extra cognitive rehab or maybe one day we’ll have a drug that targets certain gene receptors. The idea is that you could divide people into different groups and use that knowledge not just for prediction but hopefully one day for improved, individualized treatment.” 

Article: Cramer SC, Parodi L, Moslemi Z, Braun RG, Aldridge CM, Shahbaba B, Rosand J, Holman EA, Investigators SS. Genetic Variation and Stroke Recovery: The STRONG Study. Stroke. 2024;55:2094-2102. doi: 10.1161/STROKEAHA.124.047643

Does the Environment Override Genes for People at Risk of Stroke?

FYI. Way too many words here for me to understand. Hope your doctor can figure this out.

Does the Environment Override Genes for People at Risk of Stroke?

Large study detects interaction between genetic susceptibility and neighborhood deprivation

by Nicole Lou, Senior Staff Writer, MedPage Today February 8, 2023

DALLAS -- Certain social determinants of health may dilute the contribution of genetics to acute ischemic stroke susceptibility in some people, according to a large-scale study.

Based on the NIH's All of Us program, an initiative to enroll 1 million people in a diverse health database for research, acute ischemic stroke risk correlated significantly with both community deprivation and personal genetic factors as indexed by the Deprivation Index and a polygenic risk score, respectively.

However, there was a significant interaction between genetic risk and neighborhood deprivation: only people in the lowest tertile of deprivation saw an effect of genetics on stroke risk (OR 1.08, 95% CI 1.02-1.15), whereas the intermediate and high deprivation groups did not see such genetic susceptibility play out in actual events (P=0.02 for interaction), reported Cyprien Rivier, MD, a postdoctoral researcher at Yale University School of Medicine in New Haven, Connecticut, during the American Stroke Association's International Stroke Conferenceopens in a new tab or window.

As only residents of privileged areas "were more susceptible to the effects of polygenic variation on the risk of ischemic stroke," Rivier speculated "that in areas of high deprivation, the environmental risk factors become more important than genetic predisposition."

Randolph Marshall, MD, of Columbia University Irving Medical Center and New York-Presbyterian Hospital in New York City, called it a "reasonable hypothesis that the genetic component is overshadowed perhaps by the other factors related to neighborhood deprivation."

Yet epigenetics may also play a role in stroke risk, given that such gene activity can be explained by socially structured stressors, suggested Marshall, speaking at the audience Q&A.

Rivier agreed with Marshall's hypothesis and said that All of Us, which includes electronic health records, biospecimens, surveys, and wearables data, doesn't include the data for epigenetic analysis.

The present cross-sectional analysis included nearly 150,000 individuals, split evenly by tertiles of neighborhood deprivation.

The Deprivation Index used in the study -- based on the Census Bureau's American Community Survey -- quantifies a neighborhood's standard of living, health, education, economic security, housing quality, and neighborhood quality.

Meanwhile, genetic factors predisposing an individual to acute ischemic stroke were aggregated in a polygenic risk score that covers 530 variants associated with important stroke risk factors, namely blood pressure, cholesterol, glucose, BMI, diet, physical activity, and smoking. These seven domains come from the American Heart Association's old "Life's Simple 7" framework, recently replaced by "Life's Essential 8"opens in a new tab or window to include sleep health.

Rivier reported that compared with residents of the most privileged neighborhoods, the most deprived individuals tended to be younger (49.3 vs 54.4 years for least deprived, P<0.001) and more likely Black (34.3% vs 6.9%, P<0.001) or Hispanic (27.1% vs 7.7%, P<0.001). They also had a higher polygenic risk score (0.11 vs -0.13, P<0.001).

The incidence of acute ischemic stroke was 1.5% in the most deprived group, significantly lower than the 2.0% for intermediate and low deprivation groups (P<0.001). However, Rivier said high deprivation actually corresponded with more strokes upon adjustment for age and other factors.

"It is important to note that our results are specific to this particular risk score and condition. We expect other combinations of genetic factors and environment to be evaluated," he cautioned.

During the session Q&A, another audience member asked if there is any implementation plan in place or next steps to put study findings into action.

Rivier acknowledged that his group does not have the expertise to implement this, but encouraged others to take this on.

• 

  Nicole Lou is a reporter for MedPage Today, where she covers cardiology news and other developments in medicine. Follow

Disclosures

The study was supported by the NIH and the American Heart Association.

Rivier had no conflicts of interest listed.

Primary Source

International Stroke Conference

Source Reference: opens in a new tab or windowRivier C "Neighborhood deprivation and polygenic contribution to acute ischemic stroke: results from the All of Us research program" ISC 2023.

Genes associated with inflammation may serve as biomarkers for the diagnosis of coronary artery disease and ischaemic stroke

Once you know you have these genes, WHAT IS THE EXACT PREVENTION PROTOCOL THAT WILL PREVENT BAD THINGS HAPPENING?

Genes associated with inflammation may serve as biomarkers for the diagnosis of coronary artery disease and ischaemic stroke

Lipids in Health and Disease — Zheng PF, Liao FJ, Yin RX, et al. | March 17, 2020

In the present study, the researchers sought to identify genes and pathways involved in coronary artery disease (CAD) and ischaemic stroke (IS) and related mechanisms. Two array CAD datasets of (GSE66360 and GSE97320) and an array IS dataset (GSE22255) have been downloaded. Using the limma package, differentially expressed genes (DEGs) were identified. In total, 20 common DEGs (all upregulated) were identified between the CAD/IS and control groups. The top 5 high degree genes, including Jun proto-oncogene (JUN, degree = 9), C-X-C motif chemokine ligand 8 (CXCL8, degree = 9), tumour necrosis factor (TNF, degree = 9), suppressor of cytokine signalling 3 (SOCS3, degree = 8) and TNF alpha induced protein 3 (TNFAIP3, degree = 8) were noted following MCODE analysis. Findings suggested that the inflammation-related CXCL8, TNF, SOCS3 and TNFAIP3 can serve as biomarkers for CAD or IS diagnosis. Possible mechanisms can include Toll-like receptor, TNF, NF-kappa B, cytokine-cytokine receptor interactions and the NOD-like receptor signalling pathways.

Read the full article on Lipids in Health and Disease

Researchers discover genes linked to resilience against brain pathologies

Not sure how I would test to see if I have these genes. 
http://www.news-medical.net/news/20170426/Researchers-discover-genes-linked-to-resilience-against-brain-pathologies.aspx

• Download PDF Copy

April 26, 2017

The pathologies (damage) in the brain that stroke, Alzheimer's disease and other neurological conditions cause in older adults only partially explain the memory loss, reduced reasoning ability and other cognitive impairments that result from these conditions. Little is known about why the effects of brain pathology vary between people who develop it.
Now researchers have discovered two genes, known as UNC5C and ENC1, that are associated with aging individuals having better memory and brain function than would be expected, given the amount of pathologies that accumulated in their brains. They reported their findings in an article published in the journal PLOS Medicine on April 24.
"Most of the cognitive loss that we experience in older age remains unexplained. Certain individuals are very resistant to the pathologies of the aging brain, while others may be particularly vulnerable," says study senior investigator David Bennett, MD, who directs the Rush Alzheimer's Disease Center.
These potentially damaging pathologies include the buildup of harmful proteins known as amyloid plaques and neurofibrillary tangles that occur in Alzheimer's disease; the protein deposits known as Lewy bodies that accompany Parkinson's disease and Lewy body dementia; and the death of massive amounts of brain cells caused by stroke.
Identifying genes that contribute to resistance to these and other brain pathologies could provide researchers with new targets for developing medications that would enhance the brains of aging adults to resist Alzheimer's disease and other neurological conditions, Bennett says.
Study used genetic analysis of 979 organ donors' brain tissue
The researchers drew on a vast trove of data, including genetic analyses, generated by two ongoing long-term studies of aging based at Rush University Medical Center, which includes study participants' donation of their brains for research after their death. These participants were tested annually to measure their cognitive function, allowing for a comparison of the decrease in cognitive function with the development of any pathology found when their brains were autopsied after their deaths.

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Using this information for 979 participants, the researchers assessed how much each person's thinking ability withstood the development of memory loss despite the accumulation of brain pathology - in other words, how resilient they were to pathology. Then they conducted a complex, multiple step analysis "to identify segments of the human genome (i.e, genes) that help us to maintain cognitive function in the face of advancing age and disease," explains study senior investigator Philip De Jager, MD, PhD, professor of neurology at Columbia University Medical Center.
The innovative approach combined an analysis of the human genome - the complete set of genes in a person -- with an evaluation of the epigenome -- changes to DNA that helps determine which genes can be "read" so its protein is made. Epigenome in part reflects how our brain responds to life experiences and exposures to environmental factors.
The analysis identified UNC5C and ENC1 as being associated with cognitive resilience. In addition, the researchers found that TMEM106B -- a gene whose presence previously had been identified as possibly protecting against age-related frontotemporal lobar degeneration -- also may play a role in brain resilience.
"These genes should be studied further to expand our understanding of molecular mechanisms relevant to cognitive resilience that could be translated into prognostic and therapeutic tools for dementia prevention," the researchers write in the paper's summary.

Source:

https://www.rush.edu/news/press-releases/genes-associated-resilience-against-brain-pathology-identified

Being Happy Is Not Just “In Your Genes” — You Need More

Does your doctor understand your mental filter (cognitive bias) to get you into a happy state even after your stroke? Does your psychologist?
 http://www.spring.org.uk/2016/07/happy-not-just-genes-need.php?omhide=true&utm_source=PsyBlog&utm_campaign=54a835224f-RSS_EMAIL_CAMPAIGN_MAILCHIMP&utm_medium=email&utm_term=0_10ef814328-54a835224f-213838825

How the same genes can be linked to both happiness and depression.

Certain genes linked to mental health can lead to both happiness and depression, a new review concludes.

It all depends on the environment in which a person is brought up.
Supportive environments can lead to positive biases in seeing the world (essentially: happiness).
Unsupportive environments can lead to the opposite.
Pr

“‘Cognitive biases are when people consistently interpret situations though particular mental ‘filters’ – when people have a cognitive bias that emphasises negative aspects or thoughts, they are more at risk of mental health disorders.
There is a lot of research about these biases, and a lot of research about genes that may make people susceptible to mental ill health.
However, we suggest that it could make more sense to bring together these two areas of research.”

Professor Fox is currently researching how genes and the environment combine to affect our cognitive filters.

Sweeping review of human genome IDs stroke risk genes

It has been two weeks since this came out, Has your doctor contacted you yet? 

Sweeping review of human genome IDs stroke risk genes

Researchers seeking to better understand how our genes contribute to stroke risk have completed what is believed to be the largest and most comprehensive review of the human genome to identify genes that predispose people to ischemic stroke, the cause of approximately 85 percent of all stroke cases.
The research has confirmed the role of the handful of genes previously suspected, ruled out others and identified a new gene that may become a drug target for doctors seeking to prevent this potentially deadly and often debilitating condition.

Massive collaboration

Stroke is the No. 2 killer worldwide, and risk factors such as smoking, high blood pressure, diabetes and high cholesterol are well established. Our genes, however, also play an important role in determining our stroke risk, but relatively little is known about the inheritable risk for ischemic stroke. (Ischemic strokes are caused by blood clots, while other forms of stroke are caused by the rupturing of blood vessels.)
To advance the understanding of ischemic stroke, a massive study has been conducted by researchers with the National Institute of Neurological Disorders and Stroke’s Stroke Genetics Network (SiGN) and the International Stroke Genetics Consortium (ISGC). The project is believed to be roughly twice as large as any previous study investigating the genetic factors contributing to ischemic stroke. The project examined the genomes of tens of thousands of stroke patients and far more control subjects. It represents the work of researchers around the world, including doctors and scientists at the University of Virginia Health System.

The study involved many research sites from around the United States and Europe.

“We have started to alter the mortality from stroke, which is great and exciting,” said Bradford Worrall, MD, a top stroke expert at UVA and a leader of the project. “However, if you look at all the known risk factors, they are fairly poor at predicting an individual’s risk. There’s some statistics that suggest as much as 50 percent of the residual risk is unexplained, which is why understanding the underlying genetic contributors is so important.”

Understanding ischemic stroke

Ischemic stroke actually represents a collection of several different stroke subtypes, including strokes caused by blood clots that form in or near the heart and strokes that result from hardening of the arteries (atherosclerosis) in the head or neck. The new gene identified by the study, for example, is thought to be associated with strokes that result from large artery atherosclerosis.
The study also shed light on the only gene that has been linked to all forms of ischemic stroke. By taking a highly sophisticated approach to the genetic analysis, the researchers were able to show that the gene appears to have the strongest effect in strokes related to small vessel disease. This suggests that each identified stroke gene so far is associated with a specific stroke subtype, the researchers report.
“That shifts the research landscape a little bit in terms of how we investigate that finding going forward,” Worrall said. “We’ll probably need to think about that as both a subtype-specific [risk factor] and – possibly – a general risk factor for stroke.”

Findings published

The findings have been published online by the scientific journal Lancet Neurology. The SiGN study was funded by the National Institutes of Health’s National Institute of Neurological Disorders and Stroke, grant No. U01 NS069208.

Sweeping Review of Human Genome IDs Stroke Risk Genes

Followup research won't occur from our fucking failures of stroke associations.
https://news.virginia.edu/content/sweeping-review-human-genome-ids-stroke-risk-genes

Researchers seeking to better understand how our genes contribute to stroke risk have completed what is believed to be the largest and most comprehensive review of the human genome to identify genes that predispose people to ischemic stroke, the cause of approximately 85 percent of all stroke cases.
The project examined the genomes of tens of thousands of stroke patients and far more control subjects. It represents the work of researchers around the world, including doctors and scientists at the University of Virginia Health System.
The research has confirmed the role of the handful of genes previously suspected, ruled out others and identified a new gene that may become a drug target for doctors seeking to prevent this potentially deadly and often debilitating condition.
Stroke is the No. 2 killer worldwide, and risk factors such as smoking, high blood pressure, diabetes and high cholesterol are well established. Our genes, however, also play an important role in determining our stroke risk, but relatively little is known about the inheritable risk for ischemic stroke. (Ischemic strokes are caused by blood clots, while other forms of stroke are caused by the rupturing of blood vessels.)
To advance the understanding of ischemic stroke, a massive study has been conducted by researchers with the National Institute of Neurological Disorders and Stroke’s Stroke Genetics Network – also known as SiGN – and the International Stroke Genetics Consortium. The project is believed to be roughly twice as large as any previous study investigating the genetic factors contributing to ischemic stroke.
“We have started to alter the mortality from stroke, which is great and exciting,” said Dr. Bradford Worrall, a top stroke expert at UVA and a leader of the project. “However, if you look at all the known risk factors, they are fairly poor at predicting an individual’s risk. There’s some statistics that suggest as much as 50 percent of the residual risk is unexplained, which is why understanding the underlying genetic contributors is so important.”
Ischemic stroke actually represents a collection of several different stroke subtypes, including strokes caused by blood clots that form in or near the heart and strokes that result from hardening of the arteries, or atherosclerosis, in the head or neck. The new gene identified by the study, for example, is thought to be associated with strokes that result from large-artery atherosclerosis.

The study also sheds light on the only gene that has been linked to all forms of ischemic stroke. By taking a highly sophisticated approach to the genetic analysis, the researchers were able to show that the gene appears to have the strongest effect in strokes related to small vessel disease. This suggests that each identified stroke gene so far is associated with a specific stroke subtype, the researchers report. “That shifts the research landscape a little bit in terms of how we investigate that finding going forward,” Worrall said. “We’ll probably need to think about that as both a subtype-specific [risk factor] and – possibly – a general risk factor for stroke.”
The researchers expect to continue to mine their data for new insights that will be published in future papers. They say that much more work will need to be done to bring the understanding of the genetic risk factors for ischemic stroke up to that of other common diseases. Genetics have the potential to provide insight into the underlying mechanisms of ischemic stroke and related diseases.
The current findings have been published online by the scientific journal Lancet Neurology. The SiGN study was funded by the National Institutes of Health’s National Institute of Neurological Disorders and Stroke, grant No. U01 NS069208.

Media Contact

Josh Barney

UVA Health System

jdb9a@virginia.edu 434-243-1988

- See more at: https://news.virginia.edu/content/sweeping-review-human-genome-ids-stroke-risk-genes#sthash.3h2usaLQ.dpuf

Researchers seeking to better understand how our genes contribute to stroke risk have completed what is believed to be the largest and most comprehensive review of the human genome to identify genes that predispose people to ischemic stroke, the cause of approximately 85 percent of all stroke cases.

The project examined the genomes of tens of thousands of stroke patients and far more control subjects. It represents the work of researchers around the world, including doctors and scientists at the University of Virginia Health System.

The research has confirmed the role of the handful of genes previously suspected, ruled out others and identified a new gene that may become a drug target for doctors seeking to prevent this potentially deadly and often debilitating condition.

Stroke is the No. 2 killer worldwide, and risk factors such as smoking, high blood pressure, diabetes and high cholesterol are well established. Our genes, however, also play an important role in determining our stroke risk, but relatively little is known about the inheritable risk for ischemic stroke. (Ischemic strokes are caused by blood clots, while other forms of stroke are caused by the rupturing of blood vessels.)

To advance the understanding of ischemic stroke, a massive study has been conducted by researchers with the National Institute of Neurological Disorders and Stroke’s Stroke Genetics Network – also known as SiGN – and the International Stroke Genetics Consortium. The project is believed to be roughly twice as large as any previous study investigating the genetic factors contributing to ischemic stroke.

“We have started to alter the mortality from stroke, which is great and exciting,” said Dr. Bradford Worrall, a top stroke expert at UVA and a leader of the project. “However, if you look at all the known risk factors, they are fairly poor at predicting an individual’s risk. There’s some statistics that suggest as much as 50 percent of the residual risk is unexplained, which is why understanding the underlying genetic contributors is so important.”

Ischemic stroke actually represents a collection of several different stroke subtypes, including strokes caused by blood clots that form in or near the heart and strokes that result from hardening of the arteries, or atherosclerosis, in the head or neck. The new gene identified by the study, for example, is thought to be associated with strokes that result from large-artery atherosclerosis.

Dr. Bradford Worrall is one of the leaders of the project, which sought to clarify genetic involvement in ischemic stroke.

The study also sheds light on the only gene that has been linked to all forms of ischemic stroke. By taking a highly sophisticated approach to the genetic analysis, the researchers were able to show that the gene appears to have the strongest effect in strokes related to small vessel disease. This suggests that each identified stroke gene so far is associated with a specific stroke subtype, the researchers report.

“That shifts the research landscape a little bit in terms of how we investigate that finding going forward,” Worrall said. “We’ll probably need to think about that as both a subtype-specific [risk factor] and – possibly – a general risk factor for stroke.”

The researchers expect to continue to mine their data for new insights that will be published in future papers. They say that much more work will need to be done to bring the understanding of the genetic risk factors for ischemic stroke up to that of other common diseases. Genetics have the potential to provide insight into the underlying mechanisms of ischemic stroke and related diseases.

The current findings have been published online by the scientific journal Lancet Neurology. The SiGN study was funded by the National Institutes of Health’s National Institute of Neurological Disorders and Stroke, grant No. U01 NS069208.

Media Contact

Josh Barney

UVA Health System

jdb9a@virginia.edu 434-243-1988

Study identifies common genetic variants that double risk for blood clots in african americans

Be careful out there. VTE -

Venous Thromboembolism(Deep Venous Thrombosis & Pulmonary Embolism)

http://www.mdlinx.com/internal-medicine/top-medical-news/article/2016/02/22/3

American Society of Hematology News

One in three African Americans have at least one variant that increases risk.
New research published online in Blood identifies common genetic variants predominantly found in African Americans that double their risk for blood clots. To understand the genetic risk factors for VTE specific to African Americans, a team of researchers led by Dr. Perera conducted a genome–wide association study in which they genotyped DNA samples from 578 African Americans, 146 of whom had a history of unprovoked VTE. Next, they confirmed the variants deemed highly prevalent in the first group by genotyping an additional group of 159 African Americans, including 94 with VTE. Based on their analysis, researchers identified a link between VTE and three variants in a chromosome associated with decreased expression of thrombomodulin, a protein that regulates clotting: rs2144940, rs2567617, and rs1998081. Investigators suggest that the presence of one of these three variants doubles the risk for VTE. Approximately 36 percent of African Americans have at least one of these variants. Surprisingly, these variants were found in much lower frequency in other ethnicities from previous studies. “This study not only brings us closer to understanding the cause of VTE in African Americans, it demonstrates the importance of conducting population–specific research in precision medicine,” said Dr. Perera. “Our next steps will involve investigating the predictiveness of these risk factors for VTE with the goal of reducing the high prevalence and burden of VTE in this disproportionately affected population.”

Four key studies that link coffee to heart attacks and hypertension

This seems to follow the same course as alcohol consumption. Only those with the proper genetic marker benefit. But your doctor will unlikely ever do gene testing prior to telling you coffee is bad for you because it raises your blood pressure. I most assuredly will not get gene testing to see if I'm in the right category. 

Four key studies that link coffee to heart attacks and hypertension

Is drinking coffee good for you? Some research indicates that that simple question cannot be answered without knowing something about your DNA.
Maybe the clearest evidence that genetics determines caffeine metabolism arises from a study of twins, published in 2002, that indicates that the speed with which a person processes caffeine is largely heritable.
At the same time, other studies have identified a single nugget of our DNA that seems to determine whether we process caffeine quickly or slowly. That, in turn, appears to have a large effect on whether coffee is good for your health.
For those who process caffeine slowly, this line of research indicates, drinking coffee raises the risks of heart attacks and high blood pressure. For those who process it quickly, drinking coffee seems to be safe - it may even protect against a heart attack or high blood pressure.
While researchers caution that more work needs to be done, they suggest that giving the public a general guideline regarding coffee doesn’t make sense. People are too different.
Here are some of the highlights in this line of research.
For the key studies in favor of coffee, try this.
“The interindividual differences in the 3-demethylation of caffeine alias CYP1A2 is determined by both genetic and environmental factors.”
Pharmacogenetics, August 2002.
http://www.ncbi.nlm.nih.gov/pubmed/12172216
Finding: Forty-nine identical twins and 34 fraternal twins were given 200 milligrams of caffeine; six hours later, a urine sample was taken. Those sample were then analyzed to see how quickly each person had broken down, or metabolized, the caffeine. In identical twins, the rates of metabolism were about twice as correlated as they were in fraternal twins. The scientists concluded that genetics largely determines the rate at which a person processes caffeine.
“CYP1A2 phenotype and genotype in a population from the Carboniferous Region of Coahuila, Mexico.”
Toxicology Letters, April 2005
http://www.ncbi.nlm.nih.gov/pubmed/15763632
Finding: Scientists in Mexico gave 46 volunteers a cup of instant coffee containing 140 milligrams of caffeine. Eight hours later, urine samples were collected. Those subjects who had one variant of the CYP1A2 gene processed caffeine more than twice as quickly as those who had the other, researchers found. Other similar efforts in China and Germany found a link between the gene and caffeine metabolism, predominantly in smokers.
“Coffee, CYP1A2 Genotype, and Risk of Myocardial Infarction”
JAMA, March 2006
http://www.ncbi.nlm.nih.gov/pubmed/16522833
Finding: Researchers compared about 2,000 people in Costa Rica who had a heart attack with 2,000 others who had not, examining both how much coffee they drank, as well as their DNA. In those subjects with the genetic marker indicating slow caffeine metabolism, the chance of heart attack appeared to rise with each cup of coffee. By contrast, those subjects with the genetic marker for rapid caffeine metabolism had a lower chance of heart attack with each cup.
The authors concluded: “Intake of coffee was associated with an increased risk of nonfatal [heart attack] only among individuals with slow caffeine metabolism, suggesting that caffeine plays a role in this association.”
“CYP1A2 genotype modifies the association between coffee intake and the risk of hypertension”
Journal of Hypertension, August 2009.
http://www.ncbi.nlm.nih.gov/pubmed/19451835
Finding: Researchers looked at the genetics, blood pressure and coffee habits of 553 young Italian over more than eight years. As with heart attacks (see above), the effects of coffee diverged depending on a person’s genetics.
For those with the gene for slow caffeine metabolism, the risks of high blood pressure rose dramatically with coffee intake. For those with the gene for rapid caffeine metabolism, the risk of high blood pressure dropped with coffee intake.
The authors concluded: People with the slower caffeine metabolism “are at increased risk and should thus abstain from coffee.” On the other hand, people with the genetics for the rapid caffeine metabolism “can safely drink coffee.”

Why Some People React More Emotionally To Life’s Ups and Downs

So maybe your doctor could test for this to see if this would make you more susceptible to PTSD. And provide protocols to prevent that from happening.
http://www.spring.org.uk/2015/05/why-some-people-react-more-emotionally-to-lifes-ups-and-downs.php?utm_source=PsyBlog
Professor Rebecca Todd who led the study, said:

“People really do see the world differently.
For people with this gene variation, the emotionally relevant things in the world stand out much more.”

The gene is called ADRA2b and it regulates the neurotransmitter norepinephrine

Gene that reduces risk of stroke discovered

I tore one of my carotid arteries, so I wonder if I don't have this gene or I was so violent that it overcame any protective effect this had.
There is also this blood clotting gene you may want to know about.

New stroke gene discovery could lead to tailored treatments

And this one;  alteration in a gene called HDAC9 which affects a person's risk of large artery ischemic stroke. 

Genetic variant increases risk of common type stroke

The newest article here;

http://www.allvoices.com/article/100002571
Now new research by a team made up of Royal Holloway researchers together with colleagues drawn from the US and Europe offers some hope of reducing these appalling statistics.
Two pairs of major arteries in the neck, the carotid and the vertebral arteries, together called the cervical arteries, carry blood to the brain. The researchers found that people possessed of a specific variant of a gene, called Phosphatase and Actin Regulator 1 or PHACTR1 for short, are less likely to suffer a cervical artery dissection, a tear in the lining of one of these arteries. Such a tear can lead to compression of adjacent nerves and make a sufferer more likely to develop blood clots that can cause blockage of blood vessels thus restricting blood supply to the brain, so leading to a stroke.
The discovery of these beneficial properties of PHACTR1 could prompt the development of new treatments and prevention strategies for the disease, which is a major cause of stroke in young adults. The PHACTR1 gene variant has also been identified as one that protects against migraines and affects the risk of heart attack.

More at link.

Coffee-drinking Genes Identified

So do those with these genes have a lower chance of dementia because of this?
Coffee May Lower Your Risk of Dementia

http://www.biosciencetechnology.com/news/2014/10/coffee-drinking-genes-identified?et_cid=4195077&et_rid=648870051&type=headline

Scientists Unlock Key to Blood Vessel Formation

Since we need new blood vessels to supply the all the neurogenesis that is occurring your doctor should be figuring out a way to handle this post-stroke. At least you hope your doctor is the one that correctly figures out how to do this out of the thousands of doctors working on it.
http://www.biosciencetechnology.com/news/2014/08/scientists-unlock-key-blood-vessel-formation?

Researchers Find Gene Critical for Development of Brain Motor Center

Well this is so simple, you follow this research to its natural conclusion. How can we use this to redevelop dead and damaged brains from stroke?
http://www.biosciencetechnology.com/news/2014/06/researchers-find-gene-critical-development-brain-motor-center?
In a report published in Nature Communications, an Ottawa-led team of researchers describe the role of a specific gene, called Snf2h, in the development of the cerebellum. Snf2h is required for the proper development of a healthy cerebellum, a master control centre in the brain for balance, fine motor control and complex physical movements.
Athletes and artists perform their extraordinary feats relying on the cerebellum. As well, the cerebellum is critical for the everyday tasks and activities that we perform, such as walking, eating and driving a car. By removing Snf2h, researchers found that the cerebellum was smaller than normal, and balance and refined movements were compromised.
Led by Dr. David Picketts, a senior scientist at the Ottawa Hospital Research Institute and professor in the Faculty of Medicine at the University of Ottawa, the team describes the Snf2h gene, which is found in our brain's neural stem cells and functions as a master regulator. When they removed this gene early on in a mouse's development, its cerebellum only grew to one-third the normal size. It also had difficulty walking, balancing and coordinating its movements, something called cerebellar ataxia that is a component of many neurodegenerative diseases.
"As these cerebellar stem cells divide, on their journey toward becoming specialized neurons, this master gene is responsible for deciding which genes are turned on and which genes are packed tightly away," said Dr. Picketts. "Without Snf2h there to keep things organized, genes that should be packed away are left turned on, while other genes are not properly activated. This disorganization within the cell’s nucleus results in a neuron that doesn't perform very well—like a car running on five cylinders instead of six."
The cerebellum contains roughly half the neurons found in the brain. It also develops in response to external stimuli. So, as we practice tasks, certain genes or groups of genes are turned on and off, which strengthens these circuits and helps to stabilize or perfect the task being undertaken. The researchers found that the Snf2h gene orchestrates this complex and ongoing process. These master genes, which adapt to external cues to adjust the genes they turn on and off, are known as epigenetic regulators.
"These epigenetic regulators are known to affect memory, behaviour and learning," said Dr. Picketts. "Without Snf2h, not enough cerebellar neurons are produced, and the ones that are produced do not respond and adapt as well to external signals. They also show a progressively disorganized gene expression profile that results in cerebellar ataxia and the premature death of the animal."
There are no studies showing a direct link between Snf2h mutations and diseases with cerebellar ataxia, but Dr. Picketts added that it "is certainly possible and an interesting avenue to explore."
In 2012, Developmental Cell published a paper by Dr. Picketts' team showing that mice lacking the sister gene Snf2l were completely normal, but had larger brains, more cells in all areas of the brain and more actively dividing brain stem cells. The balance between Snf2l and Snf2h gene activity is necessary for controlling brain size and for establishing the proper gene expression profiles that underlie the function of neurons in different regions, including the cerebellum.
This research was funded by the Canadian Institutes of Health Research and the U.S. National Institutes of Health.

New stroke gene discovery could lead to tailored treatments

Well this is a question for your researcher, how this helps you.
http://www.sciencecodex.com/new_stroke_gene_discovery_could_lead_to_tailored_treatments-106099
An international study led by King's College London has identified a new genetic variant associated with stroke. By exploring the genetic variants linked with blood clotting – a process that can lead to a stroke – scientists have discovered a gene which is associated with large vessel and cardioembolic stroke but has no connection to small vessel stroke.
Published in the journal Annals of Neurology, the study provides a potential new target for treatment and highlights genetic differences between different types of stroke, demonstrating the need for tailored treatments.
About 15 million people worldwide suffer a stroke each year. Of these, five million die and another five million are left permanently disabled, according to numbers from the World Health Organization (WHO). Risk factors for a stroke are high blood pressure, a heart rhythm disorder, high blood cholesterol, tobacco use, unhealthy diet, physical inactivity, diabetes and advancing age.
A stroke occurs when the blood supply to the brain is cut off, often due to a blood clot blocking an artery that carries blood to the brain, which then leads to brain cell damage. Coagulation (blood clotting) abnormalities, particularly easy clotting of the blood, are therefore common contributing factors in the development of stroke.
Dr Frances Williams, Senior Lecturer from the Department of Twin Research and Genetic Epidemiology at King's and lead author of the paper, said: 'Previous studies have demonstrated the influence of genetic factors on the components of coagulation. The goal of this study was to extend these observations to determine if they were further associated with different types of stroke.'
The research was carried out in three stages. The first consisted of a genome-wide association study (GWAS) in 2100 healthy volunteers which identified 23 independent genetic variants that were involved in coagulation. The second stage examined the 23 variants in 4200 stroke and non-stroke cases from centres across Europe (Wellcome Trust Case Control Consortium 2 and MORGAM collections) and found that a particular mutation on the ABO gene was significantly associated with stroke.
Stage three of the study used the MetaStroke cohort, a project of the International Stroke Genetics Consortium which comprises 8900 stroke cases recruited from centres in the Europe, USA and Australia, whose DNA has been collected and undergone GWA scan. It was confirmed that a variant in the ABO blood type gene was associated with stroke, a finding specific to large vessel and cardioembolic stroke.
Dr Williams said: 'The discovery of the association between this genetic variant and stroke identifies a new target for potential treatments, which could help to reduce the risk of stroke in the future. It is also significant that no association was found with small vessel disease, as this suggests that stroke subtypes involve different genetic mechanisms which emphasises the need for individualised treatment.'

Jumping Genes in the Brain Ensure That Even Identical Twins Are Different

So lets identify some jumping genes that can reprogram themselves to take over and recreate functionality that was damaged/died during our strokes.
http://www.scientificamerican.com/article.cfm?id=what-makes-each-brain-unique

• Genes we inherit and environmental factors both influence human behaviors. Scientists have recently discovered other underlying processes at work.
• So-called jumping genes, segments of DNA that can copy and paste them­selves into new places in the genome, can alter the activity of full-length genes. Occasionally they will turn on neighboring genes in these locations. That activity occurs more in the brain than other areas, resulting in different traits and behaviors, even in closely related individuals.
• These mobile genetic elements may also turn out to play a role in people’s disposition to psychiatric disorders.
• Researchers are now beginning to investigate whether jumping genes help us adapt to rapidly changing environmental conditions.

Genetic variant increases risk of common type stroke

Since I had a large ischemic stroke I should be contacted for testing to see if my genetic makeup would prove the theory. But since there is no central place for stroke info to be consolidated this means we are all on our own. If survivors were in charge there wouldn't be these holes in information.
www.sciencecodex.com/genetic_variant_increases_risk_of_common_type_stroke-85446

A genetic variant that increases the risk of a common type of stroke has been identified by scientists in a study published online in Nature Genetics today. This is one of the few genetic variants to date to be associated with risk of stroke and the discovery opens up new possibilities for treatment.

Stroke is the second leading cause of death worldwide (more than one in 10 of all deaths, and over six million deaths annually), and also in developed countries is a major cause of chronic disability. As the world's populations age the impact of stroke on wellbeing is likely to increase further.

Several different mechanisms underlie strokes. One of the most common types is when blood flow is impaired because of a blockage to one or more of the large arteries supplying blood to the brain – large artery ischemic stroke. This accounts for over a third of all strokes.

Researchers from St George's, University of London and Oxford University, working with scientists from Europe, America and Australia, in one of the largest genetic studies of stroke to date, compared the genetic make-up of 10,000 people who had suffered from a stroke with 40,000 healthy individuals. The study was funded by the Wellcome Trust.

The researchers discovered an alteration in a gene called HDAC9 which affects a person's risk of large artery ischemic stroke. This variant occurs on about 10 per cent of human chromosomes. Those people who carry two copies of the variant (one inherited from each parent) have nearly twice the risk for this type of stroke compared to those with no copies of the variant.

The protein produced by HDAC9 is already known to play a role in the formation of muscle tissue and heart development. However, the exact mechanism by which the genetic variant increases the risk of stroke is not yet known. A better understanding of the mechanism could lead to new drugs to treat or prevent stroke; however, the researchers stress that this is still some way off.

Professor Hugh Markus, from St George's, University of London, who co-led the study says: "This discovery identifies a completely new mechanism for causing stroke. The next step is to determine in more detail the relationship between HDAC9 and stroke and see whether we can develop new treatments that reduce the risk of stroke. Interestingly, there are already drugs available which inhibit the HDAC9 protein. However, it is important that we understand the mechanism involved before trialling the effects of these drugs on stroke."

The researchers went on to show that the new variant does not have the same effect on the risk of other types of stroke which include bleeding in the brain (haemorrhagic stroke).

Professor Peter Donnelly, Director of the Wellcome Trust Centre for Human Genetics in the University of Oxford, who co-led the study, says: "Our study shows that the different subtypes of stroke could involve quite different genetic mechanisms. This is really fascinating, and if it holds up more generally, will move us closer to personalised medicine, where treatments and preventions can be tailored more precisely to individual patients."

Dr Peter Coleman, Deputy Director of Research at The Stroke Association, who funded collection of some of the samples used in this study, said:

"Over a third of strokes are caused by a blockage in one of the large blood vessels supplying blood to the brain (large artery stroke). Findings from this ground breaking study appear to show a genetic link which may affect a person's risk of large vessel stroke. Further study is needed, but this research could potentially lead to new methods of screening and prevention for large vessel stroke, and ultimately, new methods of treatment."