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Study examines genetic risk factors for Alzheimer's disease

03-05-2007 · EurekAlert!

Cardiff University researchers have found evidence for new genes involved in the development of Alzheimer’s disease.

Keywords: study, examines, genetic, risk, factors, alzheimer, disease, examine, factor

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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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Largest study to investigate risk factors of autism to begin enrolling families
11-14-2007 · EurekAlert!
Researchers from Kaiser Permanente and the Centers for Disease Control and Prevention, as well as from five other sites nationwide, today will begin enrolling thousands of families in the largest study to date investigating the genetic and environmental factors that may cause autism and other developmental disabilities. Researchers hope the study will contribute to better services and treatments, and to prevention strategies. Autism affects about one in 150 children born in the US.
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New Alzheimer's findings: High stress and genetic risk factor lead to increased memory decline
08-27-2007 · EurekAlert!
High stress levels may contribute to memory loss among people at risk for developing Alzheimer's disease. The å4 variant of the apolipoprotein E (APOE) gene contributes to the risk for memory loss related to Alzheimer's disease.
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Landmark study highlights complex genetic risk factors behind type 2 diabetes
04-26-2007 · EurekAlert!
A UK collaboration of scientists has identified three new genes that predispose individuals to develop type 2 diabetes, bringing scientists a step closer towards understanding what causes this complex disease. The findings bring the total number of genes known to be involved in type 2 diabetes to nine.
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Higher death rates in kidney patients with newly recognized disease
09-28-2007 · EurekAlert!
A new study on the prevalence of NSF and its risk factors found that the disease is associated with an increased risk of dying and that gadolinium exposure is a significant risk factor for developing it.
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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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U of M-led study identifies new genetic risk factors for type 2 diabetes
04-26-2007 · EurekAlert!
Ten genetic variants associated with type 2 diabetes, a disease which impacts more than 170 million people worldwide, have been identified or confirmed by a US-Finnish team led by scientists at the University of Michigan School of Public Health.
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Genetic 'fellow traveler' discovered in Alzheimer's
06-06-2007 · EurekAlert!
A new gene that influences susceptibility to late-onset Alzheimer's disease has been identified by an international research team that analyzed the genomes of more than a thousand people with and without the disorder. The researchers identified the gene, called GAB2, as one that appears to influence the risk of Alzheimer's in people with a version of a gene called APOE, which is the best established genetic risk factor for LOAD.
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People at genetic risk for Alzheimer's age mentally just like noncarriers
01-07-2007 · EurekAlert!
Australian researchers say that a genotype that heightens the risk for Alzheimer's disease does not contribute to cognitive change during most of adulthood. The largest study of its kind has found that carriers and noncarriers show the same type and extent of normal age-related cognitive declines, decades before carriers start to more often develop symptoms of dementia. The findings suggest that the higher-risk genotype acts only in later years to layer disease on top of normal aging.
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New risk factors discovered for Alzheimer's disease
07-06-2007 · EurekAlert!
A recent study in Journal of Neuroimaging suggests that cognitively normal adults exhibiting atrophy of their temporal lobe or damage to blood vessels in the brain are more likely to develop Alzheimer's disease. Older adults showing signs of both conditions were seven-times more likely to develop Alzheimer's than their peers.
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