Posts tagged genetics
Articles and news from the latest research reports.
Biology and ideology: The anatomy of politics
An increasing number of studies suggest that biology can exert a significant influence on political beliefs and behaviours. Biological factors including genes, hormone levels and neurotransmitter systems may partly shape people’s attitudes on political issues such as welfare, immigration, same-sex marriage and war. And shrewd politicians might be able to take advantage of those biological levers through clever advertisements aimed at voters’ primal emotions.
Many of the studies linking biology to politics remain controversial and unreplicated. But the overall body of evidence is growing and might alter how people think about their own and others’ political attitudes.
“People are proud of their political beliefs,” says John Hibbing, a political scientist at the University of Nebraska–Lincoln. “We tend to think they’re the result of some rational responses to the world around us.” But in fact, a combination of genes and early experiences may predispose people to perceive and respond to political issues in certain ways. Recognizing that could help the public and politicians to develop more respect for those with opposing viewpoints.
Global Genome Effort Seeks Genetic Roots of Disease
By decoding the genomes of more than 1,000 people whose homelands stretch from Africa and Asia to Europe and the Americas, scientists have compiled the largest and most detailed catalog yet of human genetic variation. The massive resource will help medical researchers find the genetic roots of rare and common diseases in populations worldwide.
The 1000 Genomes Project involved some 200 scientists at Washington University School of Medicine in St. Louis and other institutions. Results detailing the DNA variations of individuals from 14 ethnic groups are published Oct. 31 in the journal Nature. Eventually, the initiative will involve 2,500 individuals from 26 populations.
“With this resource, researchers have a roadmap to search for the genetic origins of diseases in populations around the globe,” says one of the study’s co-principal investigators, Elaine Mardis, PhD, co-director of The Genome Institute at Washington University. “We estimate that each person carries up to several hundred rare DNA variants that could potentially contribute to disease. Now, scientists can investigate how detrimental particular rare variants are in different ethnic groups.”
Smoking and hyperactivity (ADHD) share common genetic risk factor
A variation of a particular gene may link the behaviours typical of childhood attention hyperactivity disorder, or ADHD for short, and those associated with smoking, suggests research published online in the Archives of Disease in Childhood (1, 2)
Childhood ADHD and subsequent smoking in adulthood frequently go hand in hand, say the authors, with people who have been diagnosed with ADHD more likely to start smoking early and to smoke twice as much as those without the condition.
The researchers focused on five variations in DNA sequences (single nucleotide polymorphisms or SNPs) in different genes that are strongly associated with different aspects of smoking behaviour, such as the number of cigarettes smoked every day, and taking up and quitting smoking.
Yeast model offers clues to possible drug targets for Lou Gehrig’s disease
Amyotrophic lateral sclerosis, also called Lou Gehrig’s disease, is a devastatingly cruel neurodegenerative disorder that robs sufferers of the ability to move, speak and, finally, breathe. Now researchers at the Stanford University School of Medicine and San Francisco’s Gladstone Institutes have used baker’s yeast — a tiny, one-celled organism — to identify a chink in the armor of the currently incurable disease that may eventually lead to new therapies for human patients.
“Even though yeast and humans are separated by a billion years of evolution, we were able to use the power of yeast genetics to identify an unexpected potential drug target for ALS,” said Aaron Gitler, PhD, an associate professor of genetics at Stanford. “Many neurodegenerative disorders such as ALS, Parkinson’s and Alzheimer’s exhibit protein clumping or misfolding within the neurons that is thought to either cause or contribute to the conditions. We are trying to figure out why these proteins aggregate in neurons in the brain and spinal cord, and what happens when they do.”
In 2008, Gitler received a New Innovator award from the National Institutes of Health to use yeast as a model for understanding human neurodegenerative diseases and as a way to identify new targets for drug development.
(Source: med.stanford.edu)
Genes, depression and life satisfaction
Vulnerability to major depression is linked with how satisfied we are with our lives. This association is largely due to genes.
This is the main finding of a new twin study from the Norwegian Institute of Public Health in collaboration with the University of Oslo. The researchers compared longitudinal information from identical and fraternal twins to determine how vulnerability to major depression is associated with dispositional (overall) lifetime satisfaction.
Previous studies have systematically shown that life satisfaction is considerably stable over time. People who are satisfied at any one point in life are often also satisfied at other times in their lives. This stability—the dispositional life satisfaction—is often said to reflect an underlying positive mood or a positive disposition. Previous studies have also shown that people with such a positive disposition are less depressed, but very few studies have examined the mechanisms behind this relationship.
Results
• Both men and women who met the criteria for lifetime major depression (15.8% and 11.1% respectively) reported lower life satisfaction.
• 74% of the relationship between major depression and life satisfaction could be explained by genes.
• The remaining association (26%) could be explained by unique environmental factors.
• The researchers also calculated the heritability of dispositional life satisfaction and major depression separately. The heritability of dispositional life satisfaction, which has not previously been reported, was estimated to be 72%. In other words, it is largely genes that explain why we differ in our tendency to be satisfied and content with our lives.
• Major depression had a heritability of 34%, which is highly consistent with previous studies.
“The stable tendency to see the bright side of life is associated with lower risk of major depression because some genetic factors influence both conditions”, says researcher Ragnhild Bang Nes from the Division of Mental Health. Genes involved in satisfaction and positivity thus give protection against major depression. Nes is the main author of the study that was recently published in the Journal of Affective Disorders.
Susceptibility to both depression and overall life satisfaction is partly influenced by the same set of genes, but is also influenced by genes that are unique to each.
“The heritability figures mean that 72% of the individual differences in overall satisfaction, and 34% of the differences in depression, are caused by genes. These figures do not provide information on the importance of specific genes for an individual’s life satisfaction or risk of major depression. Traits and propensities like dispositional life satisfaction and vulnerability to major depression are not heritable in themselves. Heritability refers to the importance of genes for explaining the differences between people and the estimates may vary across time and place”, explains Nes.
Although the heritability of major depression was lower than that of life satisfaction, this does not necessarily mean that life satisfaction is far more heritable than depression. The researchers used questionnaire data from two time points to measure dispositional life satisfaction, and a single clinical interview to measure the prevalence of lifetime major depression. The use of only a single assessment to measure depression may partly explain why the heritability of depression is so much lower than life satisfaction.
Can we prevent depression by promoting life satisfaction?
“We found that depression and life satisfaction did not share as many environmental factors as genetic factors. This means that environmental factors of importance to life satisfaction (for example, activities and interventions that make you happy and content) only to a small extent protect against depression”, says Nes.
“Although our underlying disposition to life satisfaction and positivity appears to be relatively stable, small actions in our daily lives may provide temporary pleasures, and these are also important. How we spend our time is tremendously important for our happiness and well-being. It is therefore important to encourage and follow up on activities that make us happy”.
Nes adds:
“To some extent, positive experiences may also accumulate over time and create favorable conditions for our quality of life”.
(Source: fhi.no)
Protein regulation linked to intellectual disability
Genetics researchers at the University of Adelaide have solved a 40-year mystery for a family beset by a rare intellectual disability - and they’ve discovered something new about the causes of intellectual disability in the process.
While many intellectual disabilities are caused directly by a genetic mutation in the so-called “protein coding” part of our genes, the researchers found that in their case the answer laid outside the gene and in the regulation of proteins.
Protein regulation involves the switching on or off of a protein by specific genes. As a consequence in this case, either too much or too little of this protein can trigger the disability.
The team has studied a large (anonymous) Australian family of 100 people, who for generations have not known the source of their genetically inherited condition.
The disability - which results in a lower IQ, behavioural problems such as aggression, and memory loss, and is linked with developmental delays, epilepsy, schizophrenia and other problems - affects only the male family members and can be passed on by the female family members to their children.
Genetic samples taken from the family and laboratory testing involving mice have confirmed that the protein produced by the HCFC1 (host cell factor C1) gene is the cause of this disability.
"The causes of intellectual disability generally are highly variable and the genetic causes in particular are numerous. The vast majority of intellectual disabilities are due to genetic mutations in proteins, so it was rather unexpected that we found this particular disability to be due to a regulatory mutation," says the leader of the study, Professor Jozef Gecz from the University of Adelaide’s School of Paediatrics and Reproductive Health.
"We’ve been researching this specific disability for 10 years and it’s taken us the last three years to convince ourselves that the protein regulation is the key," he says.
"For the family, this means we now have a genetic test that will determine whether or not a female member of the family is a carrier, which brings various benefits for the family.
"From a scientific point of view, this widens our viewpoint on the causes of these disabilities and tells us where we should also look for answers for those families and individuals without answers.
"This is just the tip of the iceberg in understanding the impact of altered gene regulation on intellectual disability - the gene regulatory landscape is much bigger than the protein coding landscape. We have already found, and I would expect to continue finding, a number of other intellectual disabilities linked with protein regulation over the next 20 years or so."
Professor Gecz and his team have published their findings in this month’s issue of the American Journal of Human Genetics.
(Source: adelaide.edu.au)
Scientists deepen genetic understanding of MS
Five scientists, including two from Simon Fraser University, have discovered that 30 per cent of our likelihood of developing Multiple Sclerosis (MS) can be explained by 475,806 genetic variants in our genome. Genome-wide Association Studies (GWAS) commonly screen these variants, looking for genetic links to diseases.
Corey Watson, a recent SFU doctoral graduate in biology, his thesis supervisor SFU biologist Felix Breden and three scientists in the United Kingdom have just had their findings published online in Scientific Reports. It’s a sub-publication of the journal Nature.
An inflammatory disease of the central nervous system, MS is the most common neurological disorder among young adults. Canada has one of the highest MS rates in the world.
Watson and his colleagues recently helped quantify MS genetic susceptibility by taking a closer look at GWAS-identified variants in the major histocompatibility complex (MHC) region in 1,854 MS patients. The region has long been associated with MS susceptibility.
The MS patients’ variants were compared to those of 5,164 controls, people without MS.
They noted that eight percent of our 30-per-cent genetic susceptibility to MS is linked to small DNA variations on chromosome 6, which have also long been associated with MS susceptibility.
The MHC encodes proteins that facilitate communication between certain cells in the immune system. Outside of the MHC, a good majority of genetic susceptibility can’t be nailed down because current studies don’t allow for all variants in our genome to be captured.
“Much of the liability is unaccounted for because current research methods don’t enable us to fully interrogate our genome in the context of risk for MS or other diseases,” says Watson.
The researchers believe that one place to look for additional genetic causes of MS may be in genes that have variants that are rare in the population. “The importance of rare gene variants in MS has been illustrated in two recent studies,” notes Watson, now a postdoctoral researcher at the Mount Sinai School of Medicine in New York.
“But these variants, too, are generally poorly represented by genetic markers captured in GWAS, like the one our study was based on.”
(Source: sfu.ca)
Computer Simulation Shows Grandmas Made Humans Live Longer
Computer simulations provide new mathematical support for the “grandmother hypothesis” – a famous theory that humans evolved longer adult lifespans than apes because grandmothers helped feed their grandchildren.
“Grandmothering was the initial step toward making us who we are,” says Kristen Hawkes, a distinguished professor of anthropology at the University of Utah and senior author of the new study published Oct. 24 by the British journal Proceedings of the Royal Society B.
The simulations indicate that with only a little bit of grandmothering – and without any assumptions about human brain size – animals with chimpanzee lifespans evolve in less than 60,000 years so they have a human lifespan. Female chimps rarely live past child-bearing years, usually into their 30s and sometimes their 40s. Human females often live decades past their child-bearing years.
The findings showed that from the time adulthood is reached, the simulated creatures lived another 25 years like chimps, yet after 24,000 to 60,000 years of grandmothers caring for grandchildren, the creatures who reached adulthood lived another 49 years – as do human hunter-gatherers.
The grandmother hypothesis says that when grandmothers help feed their grandchildren after weaning, their daughters can produce more children at shorter intervals; the children become younger at weaning but older when they first can feed themselves and when they reach adulthood; and women end up with postmenopausal lifespans just like ours.
By allowing their daughters to have more children, a few ancestral females who lived long enough to become grandmothers passed their longevity genes to more descendants, who had longer adult lifespans as a result.
Placebo’s Effect May Depend on Your Genes
Your response to placebos, or dummy medicine, may depend on your genes, according to a new study.
People with a gene variant that codes for higher levels of the brain chemical dopamine respond better to placebos than those with the low-dopamine version.
The findings, reported online Oct. 23 in the journal PLoS One, could help researchers design medical studies that distinguish the placebo response from the underlying effect of a medicine — the real aim of drug trials.
New epilepsy gene discovered
In a national research partnership, Dr Sarah Heron from the University of South Australia’s Sansom Research Institute, epilepsy research group, has been working to map the genes responsible for a rare form of epilepsy - autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE).
Dr Heron and her team’s latest research to identify a new gene for this form of epilepsy has been published in Nature Genetics this month.
She says while ADNFLE affects a relatively rare group of people, the symptoms and impact of the condition can be devastating.
“ADNFLE usually develops in childhood and characterised by clusters of seizures during sleep,” Dr Heron says.
“It can have an association with cognitive deficits and or psychiatric comorbidity.
“Our research has identified that mutations in the sodium-gated potassium channel gene KCNT1 cause severe autosomal dominant nocturnal frontal lobe epilepsy and associated intellectual and or psychiatric disability.”
Dr Heron says the identification of the gene has important implications for genetic counselling and also for understanding more about the full spectrum of epilepsy disorders.