How Much of My Lifespan is Genetic? Landmark Study Has a New Answer by Super Age

 

 I think I'm well prepared to get to 100, only 30 years to go, which will mean I'll be disabled for half my life, stroke at age 50.

My genes are good: My mom at 96 is still going strong, living alone at home. Dad at 91 died with Parkinson's dementia.

 I'll get to 100 assuming I'm not too careless, having loads of fun along the way.

Part of my Hunter S. Thompson journey; Life is short, have to accomplish a lot while still relatively young and healthy.

“Life should not be a journey to the grave with the intention of arriving safely in a pretty and well preserved body, but rather to skid in broadside in a cloud of smoke, thoroughly used up, totally worn out, and loudly proclaiming "Wow! What a Ride!”

"Your body is not a temple: It's an amusement park. Enjoy the ride." Anthony Bourdain

The latest here:

How Much of My Lifespan is Genetic? Landmark Study Has a New Answer

Study Finds Greater Role for Genetics in Driving Human Lifespan

 

 I think I'm well prepared to get to 100, only 31 years to go, which will mean I'll be disabled for half my life, stroke at age 50.

My genes are good: My mom at 96 is still going strong, living alone at home. Dad at 91 died with Parkinson's dementia.

 I'll get to 100 assuming I'm not too careless, having loads of fun along the way.

Part of my Hunter S. Thompson journey; Life is short, have to accomplish a lot while still relatively young and healthy.

“Life should not be a journey to the grave with the intention of arriving safely in a pretty and well preserved body, but rather to skid in broadside in a cloud of smoke, thoroughly used up, totally worn out, and loudly proclaiming "Wow! What a Ride!”

"Your body is not a temple: It's an amusement park. Enjoy the ride." Anthony Bourdain

The latest here:

Study Finds Greater Role for Genetics in Driving Human Lifespan

WASHINGTON, Jan 29 (Reuters) - Many factors influence how long you live, such as diet, exercise, smoking, drinking, environment and other variables. It also helps not to get hit by a dump truck. But what about your genes? That has been a contentious question for decades.

A new study ‌points to a larger role for genetics than previous research had indicated, estimating the contribution of genes to determining human lifespan at about 50%. That is roughly double what prior research concluded, and it mirrors the findings of lifespan studies in laboratory animals.

"Lifespan is undoubtedly ⁠shaped by many factors, including lifestyle, genes and, importantly, randomness - take for example genetically identical organisms raised in similar environments that die at different times," said Ben Shenhar, a doctoral student in physics at the Weizmann Institute of ‌Science in Israel and lead author of the study published on Thursday in the journal Science.

"In our work, we tried to give a handle on the amount of variance between different people that can be attributed to genetics. Our study tried to partition the longevity factors into genetics and 'everything else.' The 'everything else' is around 50% of the pile."

The researchers sought to account for a confounding factor in previous studies that used Swedish and Danish twins, most dating to the 19th century. Those twin studies did not account for deaths caused by violence, accidents, infectious diseases and other factors originating outside the body - called extrinsic mortality - that the authors of the new study said skewed earlier findings about longevity's ⁠genetic component.

The cause of death was absent in the historical data, which provided merely the age at death. So if one twin died at age 90 ​of natural causes and ⁠the other twin died at age 30 not of natural causes but due to an infectious disease such as typhus or cholera, data lacking the cause of death could provide a misleading impression about the role of heredity in lifespan.

The new study employed a mathematical formula to account for extrinsic mortality among twins. Shenhar said extrinsic mortality ‌at the time when the studied twins lived, before the era of antibiotics, was 10 times higher than today, ‌primarily because of infectious diseases that are now readily curable.

The ​researchers then validated the prediction that extrinsic deaths mask heritability by using previously ‌unanalyzed and more recent data from Sweden that included twins raised together and twins raised apart. This analysis indeed found that as extrinsic mortality falls, heritability rises.

"Identical twins raised apart share their genes, but not their environment. This helps tease apart genetics from the environment, nature from nurture," Weizmann Institute systems biologist and study senior author Uri Alon said.

Fraternal twins also are valuable in such research because they share about half their genetic makeup.

"Previous twin studies used statistical methods that work well ​for other traits - height, blood pressure, personality traits, etc. These traits are not affected by extrinsic mortality," Alon said.

"But mean lifespan is ​the ⁠one special trait that is strongly affected by extrinsic mortality. Since cause of death was not recorded for the classical twin studies, it was not corrected for," Alon said.

The conclusions may have implications for research into aging.

"Low heritability estimates may have discouraged funding ‍and research into the genetics of aging, suggesting it was largely random or environmental. Our work validates the search for genetic factors of longevity, showing that the genetic signal is strong but was previously hidden by 'noise' in the data," Shenhar said.

Genes impact lifespan in both directions. On one hand, there are debilitating genetic defects that can cause disease and shorten longevity. On the other ‌hand, there are genes that have been identified that appear to offer benefits for longevity.

"Many centenarians reach age 100 without any serious medical conditions," Shenhar said. "It's ​clear that these people have protective genes which guard against developing diseases which naturally occur with age. Some of these genes have been identified, although like most complex traits longevity is likely impacted by hundreds if not thousands of genes."

Living longer is mostly down to lifestyle but after age 80 it's down to something else

One grandma lived to 98, on Dad's side; Dad died at 91.

The other grandma died in her 70's, Mom's side; Mom still living at 95.
I'm going to beat them all.

Living longer is mostly down to lifestyle but after age 80 it's down to something else

Living longer is mostly down to lifestyle factors, but after age 80 it’s down to something else, as genetics then tend to have a greater influence on longevity. Maintaining a healthy lifestyle, including exercise and diet, can be crucial to your quality of life. However, a woman who lived beyond 90 suggested that her food and habit choices didn’t negatively impact her all that much. Science says after the first eight decades of your life, healthy lifestyle choices aren’t the only thing that can make you live longer.

Living longer is down to lifestyle before genetics take over. A grandmother, Cheryl Downes, lived to 97 years old and claimed that she loved drinking beer and eating sugary snacks like ice cream and cookies until the very end. So why didn’t this impact her badly? Another woman, known as the oldest woman in Europe, claimed that the secret to living to 115 years old was ‘avoiding’ arguments. While these are both interesting points, it seems that, in the end, living a long life comes down to genetics, as opposed to diet and lifestyle. Dr. Sanjay Gupta spoke to CNN on how researchers estimate that genetics have around a 20% influence on our longevity. So, even if you don’t naturally have amazing genetic makeup, you can still do things in your control to help lead a longer and healthier life. LIVE LONGER:11 minutes of walking a day could reduce risk of early death from heart attacks and strokes. By implementing healthy habits like fitness, especially weight resistance exercise, avoiding smoking, getting enough sleep, and eating the correct diet, you can significantly mitigate your genetic risk for early death Although, lifestyle factors are especially crucial in the first seven/eight decades of your life. After that, scientists believe that genetics tend to take on a larger role.

This scientific fact may explain what was supporting Cheryl’s long life, despite the ice cream and cookie consumption. Living longer is mostly down to lifestyle but after age 80 it's down to something else. The FocusStudy shows genetics impact on lifespan. Researchers at The Jackson Laboratory conducted a pivotal study into aging and lifespan to uncover new details about how diets might make people live longer – but also their negative side effects. Within the findings, researchers found that genetic factors had a far greater impact on lifespan than diets. This highlights how underlying genetic features, yet to be identified, play a major role in how these diets would affect an individual person’s health trajectory.22 Things That Are Less Important As You Age #aging #oldisgold (ChaChingQueen)22 Things That Are Less Important As You Age #aging #oldisgold Moreover, they pinpointed genetically encoded resilience as a critical factor in lifespan. Gary Churchill, who was part of leading the study, stated: “If you want to live a long time, there are things you can control within your lifetime such as diet, but really what you want is a very old grandmother.”

ADVANCES IN STROKE: Genetics, Genomics, and Precision Medicine

 

I can see almost no use for this, survivors can't change their genes to help recovery. Useless.

ADVANCES IN STROKE: Genetics, Genomics, and Precision Medicine

James F. Meschia

,

Martin Dichgans

Originally published2 Sep 2021https://doi.org/10.1161/STROKEAHA.121.033966Stroke. ;0:STROKEAHA.121.033966

 

International stroke genetics consortium recommendations for studies of genetics of stroke outcome and recovery

I can see absolutely no use for this, survivors can't change their genes to help recovery. Useless.

International stroke genetics consortium recommendations for studies of genetics of stroke outcome and recovery 

Show all authors

Arne G Lindgren, Robynne G Braun, Jennifer Juhl Majersik, ...

First Published April 26, 2021 Case Report Find in PubMed 

https://doi.org/10.1177/17474930211007288

Article information

  

Abstract

Numerous biological mechanisms contribute to outcome after stroke, including brain injury, inflammation, and repair mechanisms. Clinical genetic studies have the potential to discover biological mechanisms affecting stroke recovery in humans and identify intervention targets. Large sample sizes are needed to detect commonly occurring genetic variations related to stroke brain injury and recovery. However, this usually requires combining data from multiple studies where consistent terminology, methodology, and data collection timelines are essential. Our group of expert stroke and rehabilitation clinicians and researchers with knowledge in genetics of stroke recovery here present recommendations for harmonizing phenotype data with focus on measures suitable for multicenter genetic studies of ischemic stroke brain injury and recovery. Our recommendations have been endorsed by the International Stroke Genetics Consortium.(Really? Then you need better people on that consortium.)

Keywords Data collection, genetics, ischemic stroke, outcome, phenotype, recovery, standardization

Introduction

Genetic studies can potentially discover biological mechanisms affecting stroke recovery with treatment implications. However, they need large sample sizes only achievable by combining data from multiple studies, where harmonized terminology, methodology, and data collection timelines are essential.

The terms stroke outcome and stroke recovery differ in meaning. Stroke outcome describes the degree of function at specific time points; stroke recovery encompasses the degree of improvement (or deterioration) over time and better captures dynamic biological processes. Stroke recovery evaluation requires initial stroke severity data, without which only stroke outcome is measurable. It is also important to distinguish restitution (“true”) recovery from behavioral compensation. For example, “true” motor recovery suggests restoration of pre-stroke movement patterns¹ whereas “compensation,” implies new (possibly dysfunctional) movement patterns for accomplishing functional tasks.²

The dynamics of stroke recovery depend on intrinsic and extrinsic factors.³ Each patient’s recovery pattern uniquely reflects the combined influences of lesion size and location, biological mechanisms of brain repair, comorbidities, pre-morbid health status, and post-stroke factors including acute recanalization, rehabilitation, psychosocial factors, and environmental influences. Consequently, the degree of stroke recovery varies considerably between individuals, and even skilled clinicians have difficulty making accurate recovery predictions.⁴

The need for improved predictive models of stroke recovery has become a major research focus^5,6 and recent studies suggest that genetic variations influence recovery after stroke.^7–9 Despite multiple studies, findings remain heterogeneous, due to differences in populations, recovery metrics, assessment time points, and study designs. Most studies using global assessments incorporate the modified Rankin Scale (mRS)¹⁰ while some use more detailed modality-specific functions, for example, upper extremity (UE) motor function, language or cognitive function,^3,11 or patient-reported outcome measures (PROMs). Few studies use repeated measures, leading to knowledge gaps on stroke recovery time course. To standardize timing and metric choices across studies, the Stroke Recovery and Rehabilitation Roundtable taskforce in 2017 recommended core outcomes for trials and standardized measurement time points to reduce heterogeneity.¹¹

Here, we focus specifically on design of prospective genetic studies of ischemic stroke (IS) recovery, aiming to ascertain the underlying genetic influences on stroke recovery biology. Our recommendations complement existing advise for standardizing phenotype data¹² and biological sample collection¹³ for stroke risk and recovery studies^11,14 by providing recommendations for pre-specified harmonized data sets suitable for large, high-quality, multi-center collaborations in prospective stroke genetic recovery studies. We propose measures comprehensive enough to provide both stroke- and domain-specific data, but simple enough to allow collection of large sample sizes across numerous and diverse enrollment sites. This will allow opportunities to discover genetic factors influencing hitherto unknown biological pathways affecting the dynamics of IS recovery. We do not here consider intracerebral hemorrhage (ICH) given ICH recovery mechanisms differ from IS.

More at link.

 

Association of coffee drinking with mortality by genetic variation in caffeine metabolism: Findings From the UK Biobank

Even if you have genes that don't process caffeine fast you're ok.

Genetics determine how much coffee you can drink before it goes wrong

Now more reasons for coffee. I bet your stroke hospital even with this information will not set up a 24 hour coffee station.  Years and years of incompetency already. Notice the 8 cups a day, I'm close to that level now that I got a new coffee maker that does 12 cups at a time. You need an accessible coffee station for that. 

Association of coffee drinking with mortality by genetic variation in caffeine metabolism: Findings From the UK Biobank

JAMA Internal Medicine — Loftfield E, et al. | July 09, 2018

In this large prospective cohort study, the researchers assessed associations of coffee drinking with mortality by genetic caffeine metabolism score. Data reported that coffee drinking was inversely linked with mortality, including among those drinking 8 or more cups per day and those with genetic polymorphisms showing slower or faster caffeine metabolism. The study findings suggested that coffee drinking can be part of a healthy diet and offers reassurance to coffee drinkers.

Methods

• The UK Biobank is a population-based study that welcomed approximately 9.2 million people from across the United Kingdom to take an interest.
• Researchers utilized baseline demographic, lifestyle, and genetic data form the UK Biobank cohort, with follow-up starting in 2006 and ending in 2016, to assess hazard ratios (HRs) for coffee intake and mortality, utilizing multivariable-adjusted Cox proportional hazards models.
• Potential effect modification was investigated by caffeine metabolism, characterized by a genetic score of previously identified polymorphisms in AHR, CYP1A2, CYP2A6, and POR that have an effect on caffeine metabolism.
• Of the 502,641 members who consented with baseline data, those who were not pregnant and had complete data on coffee intake and smoking status (n = 498,134) were included.
• Total, ground, instant, and decaffeinated coffee intake were the analyzed exposures.
• All-cause and cause-specific mortality were the main outcomes and measures.

Results

• The study results showed that the mean age of the participants was 57 years (range, 38-73 years); 271 019 (54%) were female, and 387,494 (78%) were coffee drinkers.
• It was observed that 14,225 deaths occurred over 10 years of follow-up.
• Findings revealed that coffee drinking was inversely associated with all-cause mortality.
• HRs for drinking less than 1, 1, 2 to 3, 4 to 5, 6 to 7, and 8 or more cups per day were 0.94 (95% CI, 0.88-1.01), 0.92 (95% CI, 0.87-0.97), 0.88 (95% CI, 0.84-0.93), 0.88 (95% CI, 0.83-0.93), 0.84 (95% CI, 0.77-0.92), and 0.86 (95% CI, 0.77-0.95), respectively using non–coffee drinkers as the reference group.
• Data reported that similar associations were noted for instant, ground, and decaffeinated coffee, across common causes of death, and regardless of genetic caffeine metabolism score.
• According to the findings obtained, the HRs for 6 or more cups per day ranged from 0.70 (95% CI, 0.53-0.94) to 0.92 (95% CI, 0.78-1.10), with no evidence of effect modification across strata of caffeine metabolism score (P=.17 for heterogeneity).

Read the full article on JAMA Internal Medicine

Genetics determine how much coffee you can drink before it goes wrong

Considering all the benefits of coffee what exactly is your doctor replacing it with if you have the genes that cause problems drinking too much coffee? You have to DEMAND an answer, doctors are supposed to help you, not throw up their hands in defeat. 133 posts on coffee. 65 posts on caffeine.

Genetics determine how much coffee you can drink before it goes wrong

 By Dr. Paul Sharad

The other day a patient came to see me concerned that every time he drank coffee, his heart seemed to twitch. “Is this cardiac twitch a sign of heart disease?” he asked. A doctor himself, he pointed to a study done in Zurich that suggested that drinking the equivalent of two cups of coffee reduced the body’s ability to boost blood flow to the heart muscle in response to exercise and that this caffeine effect was stronger at high altitudes. That got me a bit worried myself. Like many of us, I fancy myself an amateur barista. So how much should we be having?

The most widely used drug in the world

When it comes down to it, the main active ingredient in coffee is caffeine. Caffeine is a plant alkaloid that occurs naturally in coffee, tea, guarana and kola nuts. It’s considered the most widely used drug in the world. The good news is that caffeine improves lung function, helps glucose metabolism in the gut, aids athletic performance, and is used in medications for ailments like migraines. Many carbonated drinks also contain caffeine and when present, manufacturers automatically increase sugar content, as caffeine dulls sugar taste receptors. This increased sugar is what makes soda especially bad for you.
We metabolize caffeine at different speeds
It turns out that your “cardiac twitch” is related to your caffeine metabolism – slow metabolizers of caffeine have a higher risk of heart attacks if they drink more than two cups of coffee per day; however, fast metabolizers have a reduced risk of a heart attack if they have at least a cup of coffee a day. I suggested that I run some genetic tests on my patient (and while I was at it, I thought I’d test myself). Knowing your genetic type is important here, as when it comes to CYP1A2 and coffee, there are some interesting facts.

Your genes tell you how much coffee to drink

Those of us with the AA variant of the CYP1A2 gene are fast metabolizers, while those with the AC or CC subtypes of the gene are slow metabolizers. The risky ones are the GA or AA variants. My risk was not elevated, even if (in general) it’s best to limit caffeine to 300 to 400 milligrams each day. However, my patient had the GA variant, meaning that, if he drinks more than 200 milligrams of caffeine a day, his heart disease could end up being more than just a twitch.

Get to know your favorite beverage

The main varieties of coffee bean are Arabica or Robusta and the latter has twice the caffeine content. So how much caffeine does a cup of coffee have per cup? The results may surprise you:

• French press coffee: 100 milligrams
• Filter coffee: 150 milligrams
• Espresso coffee or cappuccino: 80 milligrams (single shot)
• Decaffeinated coffee: 8.6 milligrams
• Coke: 25-35 milligrams
• Diet Coke: 25-47 milligrams
• Red Bull: 80 milligrams (like a cup of espresso)

Bottom line

Understanding your gene type and how much caffeine is in your favorite drink is important to make sure you’re living your healthiest life – especially if you love your coffee, as your genes may have other ideas for you.

Is TBI recovery based on genetics?

Well, what is the similar answer for stroke? Is your stroke association going to do anything about this?

Cytokine Gene Polymorphisms and Outcome after Traumatic Brain Injury

To cite this article:
Ryan J. Waters, Gordon D. Murray, Graham M. Teasdale, Janice Stewart, Ian Day, Robert J. Lee, and James A.R. Nicoll. Journal of Neurotrauma. October 15, 2013, 30(20): 1710-1716. doi:10.1089/neu.2012.2792.
Published in Volume: 30 Issue 20: October 10, 2013

ABSTRACT

Clinical outcome after traumatic brain injury (TBI) is variable and cannot easily be predicted. There is increasing evidence to suggest that there may be genetic influences on outcome. Cytokines play an important role in mediating the inflammatory response provoked within the central nervous system after TBI. This study was designed to identify associations between cytokine gene polymorphisms and clinical outcome 6 months after head injury. A prospectively identified cohort of patients (n=1096, age range 0–93 years, mean age 37) was used. Clinical outcome at 6 months was assessed using the Glasgow Outcome Scale. In an initial screen of 11 cytokine gene single nucleotide polymorphisms (SNPs) previously associated with disease susceptibility or outcome (TNFA −238 and −308, IL6 −174, −572 and −597, IL1A −889, IL1B −31, −511 and +3953, and TGFB −509 and −800), TNFA −308 was identified as having a likely association. The TNFA −308 SNP was further evaluated, and a significant association was identified, with 39% of allele 2 carriers having an unfavorable outcome compared with 31% of non-carriers (adjusted odds ratio 1.67, confidence interval 1.19–2.35, p=0.003). These findings are consistent with experimental and clinical data suggesting that neuroinflammation has an impact on clinical outcome after TBI and that tumor necrosis factor alpha plays an important role in this process.

METASTROKE refines genetic stroke culprits

This one really doesn't help us directly at all, but useful for further research.

METASTROKE refines genetic stroke culprits

Gene Variants Linked to Risk of Stroke in Young Women

I don't know if this will help the young women out there but just in case you can flumox your doctor with this question. 

Gene Variants Linked to Risk of Stroke in Young Women

For release: Monday, November 06, 2006

Specific variants of a gene called phosphodiesterase 4D (PDE4D) significantly increase the risk of stroke in women aged 15-49, a new study shows. The risk is magnified in women who smoke cigarettes. The study is the first to identify a possible interaction between this gene and an environmental factor in triggering stroke. The results help to show how the gene contributes to stroke risk and may lead to new ways of preventing stroke.

"This is the first time anyone has looked at PDE4D in early-onset stroke," says Steven J. Kittner, M.D., M.P.H., of the Veterans Administration Medical Center and University of Maryland School of Maryland in Baltimore, who led the new study. The research was part of a larger effort called the Stroke Prevention in Young Women Study 2, which is designed to identify genetic and environmental risk factors for ischemic stroke (stroke that results from blockage in artery) in young women. The work was carried out in collaboration with investigators at Morehouse School of Medicine in Atlanta. It was funded in part by the National Institute of Neurological Disorders and Stroke (NINDS) and appeared in the August 15, 2006, issue of Human Molecular Genetics.*

While most strokes occur in people older than 50, about one in 5,000 women ages 15-49 suffers a stroke each year. The risk increases with smoking, obesity, diabetes, high blood pressure, and a variety of other factors. These strokes are often devastating, with long-lasting and costly effects on productivity and quality of life.

“Stroke is the third most common cause of death in the U.S. and the major cause of adult disability. Because of the large economic impact of stroke: lost lives, lost productivity, and financial burden on families and society, it is important to develop novel determinants and potential disease modifying agents for stroke. Genetic vulnerability may, at least in part, explain the excess burden of stroke in African Americans and/or the increased prevalence of stroke in women," says Richard T. Benson, M.D., Ph.D., a program director with the NINDS Office of Minority Health and Research.

"We are just entering the era when genetics studies may be able to inform us regarding the risk for a number of common diseases, including stroke,” adds program director Katrina Gwinn-Hardy, M.D., Ph.D., of the NINDS Neurogenetics Cluster.

In the study, the investigators studied 48 African-American and 48 Caucasian women to identify variations called single-nucleotide polymorphisms, or SNPs, in the PDE4D gene. Each SNP represents a variation of one DNA base, or letter, in a gene. Genes can have many SNPs. Each person inherits two copies of each gene – one from each parent – and therefore each person has two versions of every SNP.

In a second part of the study, the researchers selected 23 of the most common SNPs for analysis in 445 women between the ages of 15 and 49. About half of the participants were African-American; the other half were Caucasian. A total of 224 of the participants had suffered an ischemic stroke. The others were similar in ages and ethnicity but had not suffered a stroke.

A total of five SNPs showed significant associations with stroke in these women. The magnitude of the associations between these SNPs and stroke risk was similar in African-American and Caucasian women. It was also similar for different types of ischemic stroke.

One SNP, called rs918592, showed a particularly strong association with stroke. People with a specific variant of this SNP had a greatly increased risk of stroke if they smoked. The investigators found a strong relationship between the number of cigarettes smoked and the magnitude of the risk. People with this gene variant who smoked less than 10 cigarettes a day had approximately twice the risk of stroke as non-smokers, while people who smoked 11 or more cigarettes a day had eight times the risk. Former smokers and people who had never smoked did not have any increased risk with this gene variant.

The high-risk version of SNP 918592 was present in about 18 percent of Caucasians and 55 percent of African-Americans in the control group, Dr. Kittner says. Only participants with two copies of this version of the SNP had an increased risk of stroke.

The findings improve understanding of how the PDE4D gene may increase the risk of stroke, says Dr. Kittner. Previous reports have suggested that the gene primarily affects risk of stroke from atherosclerosis (narrowing of the arteries due to buildup of cholesterol and other substances) and cardioembolism (clots that originate in the heart and block blood flow to the brain). However, in young adults, atherosclerosis is rare. The study also found an increased risk of strokes that are not linked to atherosclerosis, and no association with cardioembolism.

It is unclear why smoking interacts with a specific variant of PDE4D to increase the risk of stroke, the investigators say. However, previous studies have shown that cigarette smoking changes the expression of many genes in the endothelium that lines blood vessels. These changes may interact with PDE4D to increase the risk of stroke. A mouse study also has shown that prenatal exposure to cigarette smoking increases the expression of PDE4D. "It is important for other studies to now look at those potential interactions," Dr. Kittner notes. However, "there is ample evidence that cigarette smoking is harmful, regardless of genotype."

While five of the SNPs investigated in this study appeared to affect the risk of stroke, there are many SNPs in the PDE4D gene and researchers may not yet have identified the most important ones for stroke risk, Dr. Kittner says. Additional studies are needed to identify other SNPs that may play a role. "Ultimately, as we learn more, we might be able to identify genetically susceptible individuals," Dr. Kittner comments. "We are far from that now, but it is one goal of this research.”

The investigators are now carrying out a study of stroke risk factors in young men using tissue samples from the NINDS Human Genetics Repository. They also are planning studies to further clarify the role of the PDE4D gene in stroke. This research could lead to development of PDE4D inhibitors or other new types of medicines that may prevent stroke.

The NINDS is a component of the National Institutes of Health (NIH) in Bethesda, Maryland, and is the nation’s primary supporter of biomedical research on the brain and nervous system. The NIH is comprised of 27 Institutes and Centers and is a component of the U. S. Department of Health and Human Services. It is the primary Federal agency for conducting and supporting basic, clinical, and translational medical research, and investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit http://www.nih.gov.