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Discovery supports theory of Alzheimer's disease as form of diabetes

Insulin may be as important for the mind as it is for the body. Recent research has raised the possibility that Alzheimer's memory loss could be due to a novel third form of diabetes. Scientists at Northwestern University have discovered why brain insulin signaling would stop working in Alzheimer's disease. They have shown that a toxic protein found in the brains of individuals with Alzheimer's removes insulin receptors from nerve cells, rendering those neurons insulin-resistant.

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Keywords: discovery, supports, theory, alzheimer, disease, form, diabetes, support, diabete

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1. 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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2. Most ancient case of tuberculosis found in 500,000-year-old human; points to modern health issues
   12-07-2007 · EurekAlert!
   Although most scientists believe tuberculosis emerged only several thousand years ago, new research from the University of Texas at Austin reveals the most ancient evidence of the disease has been found in a 500,000-year-old human fossil from Turkey.The discovery of the new specimen of the human species, Homo erectus, suggests support for the theory that dark-skinned people who migrate northward from low, tropical latitudes produce less vitamin D, which can adversely affect the immune system as well as the skeleton.
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3. Nerve fibers need specific growth factor chemical to form connections within the brain
   11-17-2006 · EurekAlert!
   A discovery on how neural circuitry develops to aid proper cerebral cortex activity may help explain the memory and cognitive decline seen in Alzheimer's disease patients -- a discovery that could point toward potential treatments, according to UC Irvine scientists.
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4. Key Function Of Nervous System Enzyme Found; Impact On Drug Development Against Alzheimer's
   09-29-2006 · ScienceDaily
   Ever since scientists first elucidated the molecular mechanisms underlying the pathology and loss of nerve cells in Alzheimer's disease, drug companies have been working to develop drugs which will inhibit the outbreak of this severe form of dementia. Now researchers in Munich and Berlin (Germany) have discovered that an enyzme which has a central causal role in Alzheimer's disease happens also to have a key function in the normal development of the nervous system. This enzyme, beta-secretase or BACE1, ensures that nerve fibers (axons) are adequately isolated with sheaths of myelin, enabling rapid conduction of electrical impulses, as well as preventing short-circuits, akin to plastic insulation on electrical wires.
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5. Less than 3 percent of UK 11-year-olds take enough exercise
   09-13-2007 · EurekAlert!
   Less than 3 percent of UK 11-year-olds are taking enough exercise, suggests research published ahead of print in the Archives of Disease in Childhood.It is recommended that kids spend at least an hour a day doing some form of moderate to vigorous physical activity, in a bid to promote good health and stave off the risks of subsequent obesity and diabetes.
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6. University of Alberta researchers report breakthrough in lowering bad cholesterol, fatty acid levels
   01-09-2008 · EurekAlert!
   Medical researchers at the University of Alberta in Edmonton, Canada have found a way to reduce the amount of bad cholesterol and fatty acids that end up in the blood from food the body metabolizes, a key discovery that could lead to new drugs to treat and reverse the effects of diabetes and heart disease related to obesity. Existing drugs called statins are used to lower cholesterol, but do not treat obesity or diabetes.
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7. Study shows cats can succumb to feline Alzheimer's disease
   12-05-2006 · EurekAlert!
   Ageing cats can develop a feline form of Alzheimer's disease, a new study reveals. Scientists at the Universities of Edinburgh, St Andrews, Bristol and California have identified a key protein which can build up in the nerve cells of a cat's brain and cause mental deterioration.
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8. 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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9. Engineered mice provide insight into Alzheimer's disease
   01-17-2008 · EurekAlert!
   One factor that determines an individual's risk of developing Alzheimer's disease is the version of the APOE gene that they carry. It has been hypothesized that increasing the amount of fat associated with apoE by overexpressing ABCA1 might decrease amyloid deposition in the brain, the hallmark of AD. Support for this hypothesis has now been generated in mice, suggesting that increasing the function of ABCA1 in the brain might benefit individuals with AD.
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10. UCSD researchers discover inflammation, not obesity, cause of insulin resistance
    11-06-2007 · EurekAlert!
    Researchers at the University of California, San Diego School of Medicine have discovered that inflammation provoked by immune cells called macrophages leads to insulin resistance and type 2 diabetes. Their discovery may pave the way to novel drug development to fight the epidemic of type 2 diabetes associated with obesity, the most prevalent metabolic disease worldwide.
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