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Tel Aviv University researcher goes "through the nose" to delay onset of Alzheimer's disease

08-17-2007 · EurekAlert!

New drug candidate dissolves plaques associated with Alzheimer's and other neurological diseases.

Keywords: tel, aviv, university, researcher, through, nose, delay, onset, alzheimer, disease

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Similar news on "Tel Aviv University researcher goes "through the nose" to delay onset of Alzheimer's disease":

Tel Aviv University researcher goes 'through the nose' to delay onset of Alzheimer's disease
08-17-2007 · EurekAlert!
New drug candidate dissolves plaques associated with Alzheimer's and other neurological diseases.
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UT medical researcher determines link between foie gras and disease
06-18-2007 · EurekAlert!
Experimental data published today by University of Tennessee Graduate School of Medicine researchers shows a potential link between foie gras consumption and amyloid-related dieases such as Alzheimer's, rheumatoid arthritis and adult onset diabetes.
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Global community listens to TAU genetic researcher at EU Conference on Hearing Loss
07-09-2007 · EurekAlert!
Is hearing loss just one of those things that happens as we get older? Tel Aviv University is working towards finding a solution to deafness that will improve the quality of life for people everywhere. This week Prof. Karen Avraham represented a European consortium, EuroHear, at an international conference in France. With her Palestinian research colleague, Prof. Avraham is a leading figure in the field of hearing loss -- her landmark research in genetics has led to improved diagnostic tests which are currently being used today.
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Research suggests new direction for ALS treatment
11-27-2007 · EurekAlert!
A research team from Wake Forest University School of Medicine is the first to show that injections of a protein normally found in human cells can increase lifespan and delay the onset of symptoms in mice with ALS, or Lou Gehrig's disease.
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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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Learning slows physical progression of Alzheimer's disease
01-23-2007 · EurekAlert!
Learning appears to slow the development of two brain lesions that are the hallmarks of Alzheimer's disease, scientists at UC Irvine have discovered. The finding suggests that the elderly, by keeping their minds active, can help delay the onset of this degenerative disease.
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Burning out? Try logging off
11-26-2007 · EurekAlert!
Electronic tethers like E-mail and cell phones have no place on vacations, says a Tel Aviv University researcher.
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Research could lead to treatment for Alzheimer's disease
04-17-2007 · EurekAlert!
A molecule designed by a Purdue University researcher could lead to the first drug treatment for Alzheimer's disease. There are many people suffering, and no effective treatment is available to them. The new molecule prevents the first step in a chain of events that leads to amyloid plaque formation in the brain.
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Less education may lead to delayed awareness of Alzheimer's onset
01-23-2008 · EurekAlert!
A review of epidemiological data has found evidence that people who spend fewer years in school may experience a slight but statistically significant delay in the realization that they're having cognitive problems that could be Alzheimer's disease.
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Alzheimer's drug based on Purdue -- designed inhibitor begins clinical trials
06-22-2007 · EurekAlert!
A drug based on the design of a Purdue University researcher to treat Alzheimer's disease began the first phase of human clinical trials this week.
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