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Research team identifies human 'memory gene'
10-19-2006 · EurekAlert!Researchers at the Translational Genomics Research Institute (TGen) today announced the discovery of a gene that plays a significant role in memory performance in humans. The study details how researchers associated memory performance with a gene called Kibra in over 1,000 individuals -- both young and old -- from Switzerland and Arizona. This study is the first to describe scanning the human genetic blueprint at over 500,000 positions to identify cognitive differences between humans.
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- Researchers identify gene involved in dog size
04-05-2007 · EurekAlert!
An international team led by researchers from the National Human Genome Research Institute, part of the National Institutes of Health, has identified a genetic variant that is a major contributor to small size in dogs. The findings appear in the April 6, 2007, issue of the journal Science.
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- Scientists identify gene that may indicate predisposition to schizophrenia
01-24-2007 · EurekAlert!
In a study from the January issue of the American Journal of Human Genetics, a research team lead by Xinzhi Zhao and Ruqi Tang (Shanghai Jiao Tong University) present evidence that genetic variation may indicate predisposition to schizophrenia. Specifically, their findings identify the chitinase 3-like 1 gene as a potential schizophrenia-susceptibility gene and suggest that the genes involved in biological response to adverse conditions are likely linked to schizophrenia.
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- Affymetrix 500K array used to identify memory gene
10-19-2006 · EurekAlert!
Affymetrix Inc., announced today that researchers at the Translational Genomics Research Institute in Phoenix, Ariz., have used the Affymetrix 500K Array to discover a gene -- called Kibra -- associated with memory performance in humans. The team's findings may be used to develop new medicines for memory-based diseases such as Alzheimer's and Parkinson's by providing scientists with a better understanding of how memory works at the molecular level.
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- Research team identifies new Alzheimer's gene
06-06-2007 · EurekAlert!
A study comparing more genetic markers in the DNA of people with and without Alzheimer's disease than ever before enabled researchers to identify a common gene that appears to increase one's risk for developing Alzheimer's disease. The finding by researchers at the Translational Genomics Research Institute, Banner Alzheimer's Institute, Kronos Science Laboratory and their collaborative partners, suggests that the gene -- called GAB2 -- modifies an individual's risk when associated with other genes, including APOE4.
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- Advance in understanding of blood pressure gene could lead to new treatments
02-04-2007 · EurekAlert!
Research by scientists at UCL (University College London) has clearly demonstrated for the first time the structure and function of a gene crucial to the regulation of blood pressure. The discovery could be important in the search for new treatments for illnesses such as heart disease, the UK's biggest killer. In a paper published online today in Nature Medicine, the team, led by Professor Patrick Vallance and Dr James Leiper, UCL Department of Medicine, reveal the role of the human gene dimethylarginine dimethylaminohydrolase (DDAH), showing that loss of DDAH activity disrupts nitric oxide (NO) production. NO is critical in the regulation of blood pressure, nervous system functions and the immune system. The role of DDAH is to break down modified amino acids (Asymmetric dimethylarginine (ADMA) and monomethyl arginine (L-NMMA)) that are produced by the body and have been shown to inhibit NO synthase. These molecules accumulate in various disease states including diabetes, renal failure and pulmonary and systemic hypertension, and their concentration in plasma (the fluid component of blood) is strongly predicative of cardiovascular disease and death. In a healthy human body, the majority of ADMA is eliminated through active metabolism by DDAH. Scientists have hypothesised that if DDAH function is impaired, NO production is reduced, and that this could be an important feature of increased cardiovascular risk. To examine this pathway in more detail, the researchers deleted the DDAH gene in mice. These mice went on to develop hypertension, or high blood pressure. They also designed specific inhibitors (small molecules) which bind to the active site of human DDAH. These small molecule inhibitors also induced hypertension in mice, confirming the importance of DDAH in the regulation of blood pressure. Dr Leiper, UCL Medicine, said: “These genetic and chemical approaches to disrupt DDAH showed remarkably consistent results, and provide compelling evidence that loss of DDAH function increases the concentration of ADMA and thereby disrupts vascular NO signalling. “There has been considerable scientific interest in this pathway and the role of ADMA as a novel risk factor, but so far there's been little evidence to support the idea that it's a cause of disease, rather than just a marker. Genes and their pathways are crucial to our understanding of cardiovascular disease and a better understanding of DDAH-1 could lead to important new treatments. “It could help us to establish if genetic variation predisposes certain people to these diseases, or whether environmental factors exert some of their effects through modulation of DDAH activity. “Our research also shows that this pathway could be harnessed therapeutically to limit production of NO in certain situations where too much nitric oxide is a bad thing; for example, hypotension and septic shock. These are some of the biggest problems in intensive care medicine and there is a huge unmet need for drug treatments.” The study, which was carried out at UCL's Rayne Institute, was funded by grants from the British Heart Foundation, the Wellcome Trust and the Medical Research Council. Professor Jeremy Pearson, Associate Medical Director of the British Heart Foundation, said: "The unexpected finding in the 1980s that a simple gas, nitric oxide (NO), is made by cells in the blood vessel wall and is a powerful control of blood vessel relaxation led to the award of the Nobel Prize in 1998 to its discoverers. "More recently, there has been increasing evidence that impairment of NO production is likely to be an important factor in the development of heart and circulatory disease, but the mechanisms responsible are not fully understood. "This study suggests for the first time that the loss of the activity of the enzyme DDAH-1 leads to reduced NO production and may cause heart and circulatory disease. These findings are likely to be important in the search for new ways to optimise the health of our blood vessels." ### Notes for Editors 1. For more information, please contact Ruth Metcalfe in the UCL Media Relations Office on tel: +44 (0)20 7679 9739, mobile: +44 (0)7990 675 947, out of hours: +44 (0)7917 271 364, e-mail: r.metcalfe@ucl.ac.uk2. 'Disruption of methylarginine metabolism impairs vascular homeostasis' is published in the February issue of the journal Nature Medicine. Advance online publication is embargoed to 18.00 GMT (13.00 US Eastern) Sunday 4 February 2007. Journalists can obtain copies of the paper by contacting the UCL Media Relations Office.3. The study was funded by the British Heart Foundation, the Wellcome Trust and the Medical Research Council. About UCL Founded in 1826, UCL was the first English university established after Oxford and Cambridge, the first to admit students regardless of race, class, religion or gender, and the first to provide systematic teaching of law, architecture and medicine. In the government's most recent Research Assessment Exercise, 59 UCL departments achieved top ratings of 5* and 5, indicating research quality of international excellence. UCL is the fourth-ranked UK university in the 2006 league table of the top 500 world universities produced by the Shanghai Jiao Tong University. UCL alumni include Mahatma Gandhi (Laws 1889, Indian political and spiritual leader); Jonathan Dimbleby (Philosophy 1969, writer and television presenter); Junichiro Koizumi (Economics 1969, Prime Minister of Japan); Lord Woolf (Laws 1954, Lord Chief Justice of England & Wales); Alexander Graham Bell (Phonetics 1860s, inventor of the telephone), and members of the band Coldplay.
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- Researchers first to map gene that regulates adult stem cell growth
01-14-2007 · EurekAlert!
A new discovery in stem cell research may mean big things for cancer patients in the future. After being the first to genetically map and identify a gene that regulates adult stem cells, the researchers investigated the gene's protein product, Latexin, which can be used to ramp up the body's stem cell count. The team's findings are being published in Nature Genetics.
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- Scientists identify a gene that may suppress colorectal cancer
03-21-2007 · EurekAlert!
In Genome Research, a husband-and-wife research team from Thomas Jefferson University report the discovery of a gene that, when mutated, may suppress colorectal cancer. To conduct the study, the researchers used a strain of mice that develop polyps, or small growths of tissue, in the digestive tract -- the harbingers of cancer. When these mice possessed one copy of the mutated gene, the incidence of small intestinal and colon polyps were reduced by about 90 percent.
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- International team identifies 480 genes that control human cell division
01-07-2008 · EurekAlert!
A team of US, Israeli and German scientists used computational biology techniques to discover 480 genes that play a role in human cell division and to identify more than 100 of those genes that have an abnormal pattern of activation in cancer cells.
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- Scripps research team sheds light on long-sought cold sensation gene
05-02-2007 · EurekAlert!
For years, scientists have struggled to identify the genes responsible for mammals' sensation of cold. Finally, scientists from The Scripps Research Institute and the Novartis Research Foundation have shown that a gene called TRPM8 is responsible for the bulk of this ability in mice.
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- U-M team identifies gene that regulates blood-forming fetal stem cells
07-26-2007 · EurekAlert!
In the rancorous public debate over federal research funding, stem cells are generally assigned to one of two categories: embryonic or adult. But that's a false dichotomy and an oversimplification. A new University of Michigan study adds to mounting evidence that stem cells in the developing fetus are distinct from both embryonic and adult stem cells.
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