New Risk Factors Discovered for Alzheimer’s Disease

Pittsburgh, Pa. – July 06, 2007 – 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.

“Alzheimer’s disease, a highly debilitating and ultimately fatal neurological disease, is already associated with other risk factors such as poor cognitive scores, education or health conditions,” says study author Caterina Rosano. “This study, because it focused on healthy, cognitively normal adults, shows that there other risk factors we need to consider.”

MRI images of participants’ brains were examined to identify poor brain circulation, damaged blood vessels and/or atrophy of the medial temporal lobe. Subjects showing any one or a combination of these symptoms were more likely to develop Alzheimer’s in the following years.

“Similarly to heart disease, brain blood vessel damage is more likely to occur in patients with high blood pressure, high cholesterol or diabetes,” says Rosano. “Since we know that prevention of these conditions can lower risk of heart attack and stroke, it is likely that it would also lower the risk of developing Alzheimer’s.”

This study is published in Journal of Neuroimaging. Media wishing to receive a PDF of this article may contact medicalnews@bos.blackwellpublishing.net.

Dr. Caterina Rosano is a physician neuroepidemiologist and assistant professor of epidemiology with the Center for Aging and Population Health at the University of Pittsburgh. She is currently developing a model to predict the incidence of cognitive and physical functional limitations in older adults. She can be reached for questions at rosanoc@edc.pitt.edu .

Journal of Neuroimaging addresses the full spectrum of human nervous system disease including stroke, neoplasia, degenerative and demyelinating disease, epilepsy, infectious disease, toxic-metabolic disease, psychoses, dementias, heredo-familial disease and trauma. Each issue offers original clinical articles, case reports, articles on advances in experimental research, technology updates, and neuroimaging CPCs. For more information, please visit http://www.blackwellpublishing.com/jon.

Wiley-Blackwell was formed in February 2007 as a result of the merger between Blackwell Publishing Ltd. and John Wiley & Sons, Inc.’s Scientific, Technical, and Medical business. Together, the companies have created a global publishing business with deep strength in every major academic and professional field. Wiley-Blackwell publishes approximately 1,250 scholarly peer-reviewed journals and an extensive collection of books with global appeal. For more information on Wiley-Blackwell, please visit http://www.blackwellpublishing.com or http://interscience.wiley.com.

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How we can stop stress from making us obese

Contact: Dr. Branwen Morgan
b.morgan@garvan.org.au
61-043-407-1326
Research Australia

Professor Herbert Herzog, Director of the Neuroscience Research Program at the Garvan Institute of Medical Research, together with scientists from the US and Slovakia, have shown that neuropeptide Y (NPY), a molecule the body releases when stressed, can ‘unlock’ Y2 receptors in the body’s fat cells, stimulating the cells to grow in size and number. By blocking those receptors, it may be possible to prevent fat growth, or make fat cells die.

“We have known for over a decade that there is a connection between chronic stress and obesity,” said Professor Herzog. “We also know that NPY plays a major role in other chronic stress-induced conditions, such as susceptibility to infection. Now we have identified the exact pathway, or chain of molecular events, that links chronic stress with obesity.”

“There is not much we can do about the increased levels of NPY caused by stress, but we can do something about the damage it causes. If we can interfere before it causes fat to amass, it could have a major impact on cardiovascular disease, diabetes, and cancer (which all have links with obesity).”

“Basically, when we have a stress reaction, NPY levels rise in our bodies, causing our heart rate and blood pressure to go up, among other things. Stress reactions are normal, unavoidable, and generally serve a useful purpose in life. It’s when stress is chronic that its effects become damaging.”

Scientists at Georgetown University (Washington D.C), part of this collaborative study, have found a direct connection between stress, a high calorie diet and unexpectedly high weight gain. Stressed and unstressed mice were fed normal diets and high calorie (high fat and high sugar, or so called ‘comfort food’) diets. The mice on normal diets did not become obese. However, stressed mice on high calorie diets gained twice as much fat as unstressed mice on the same diet. The novel and unexpected finding was that when stressed and non-stressed animals ate the same high calorie foods, the stressed animals utilised and stored fat differently.

“Our findings suggest that we may be able to reverse or prevent obesity caused by stress and diet, including the worst kind of obesity; the apple-shaped type, which makes people more susceptible to heart disease and diabetes,” says senior author of the Nature Medicine paper, Professor Zofia Zukowska of Georgetown University. “Using animal models, in which we have either blocked the Y2 receptor, or selectively removed the gene from the abdominal fat cells, we have shown that stressed mice on high calorie diets do not become obese. “Even more surprisingly, in addition to having flatter bellies, adverse metabolic changes linked to stress and diet, which include glucose intolerance and fatty liver, became markedly reduced. We do not know yet exactly how that happens, but the effect was remarkable,” she said.

Professor Herzog believes that these research findings will have a profound effect on the way society will deal with the obesity epidemic. “There are millions of people around the world who have lived with high levels of stress for so long their bodies think it’s ‘normal’. If these people also eat a high fat and high sugar diet, which is what many do as a way to reduce their stress, they will become obese.”

“Until now, the pharmaceutical industry has focused on appetite suppressants with only moderate success. Our hope is that in the near future pharmaceutical companies, using the results of our research, will develop antagonists against the Y2 receptor that will bring about a reduction in fat cells.”

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Notes to editors:

Stress-activated adipogenic pathway in fat tissue exaggerates diet-induced obesity and metabolic syndrome.
Kuo, L.E., Kitlinska, J.B., Tilan, J.U., Li, L., Baker, S.B., Johnson, M.D., Lee, E.W., Burnett, M.S., Fricke, S.T., Kvetnansky, R.K., Herzog, H. & Zukowska, Z.
Nature Medicine advance online publication, 1 July 2007

The study was co-funded by the National Institutes of Health, the American Heart Association, and the Slovak Research and Development Agency.

ABOUT GARVAN

The Garvan Institute of Medical Research was founded in 1963. Initially a research department of St Vincent’s Hospital in Sydney, it is now one of Australia’s largest medical research institutions with approximately 400 scientists, students and support staff. Garvan’s main research programs are: Cancer, Diabetes & Obesity, Arthritis & Immunology, Osteoporosis, and Neuroscience. The Garvan’s mission is to make significant contributions to medical science that will change the directions of science and medicine and have major impacts on human health. The outcome of Garvan’s discoveries is the development of better methods of diagnosis, treatment, and ultimately, prevention of disease.

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Type 1 diabetes and heart disease — Heavier may mean healthier

Contact: Michele D. Baum
BaumMD@upmc.edu
412-647-3555
University of Pittsburgh Schools of the Health Sciences

Pittsburgh scientists find more fat equals less coronary artery calcification
CHICAGO, June 23 — Researchers at the University of Pittsburgh Schools of the Health Sciences studying links between an early sign of heart disease called coronary artery calcification and body fat have found that, paradoxically, more fat may have some advantages, at least for people – particularly women – who have type 1 diabetes. Cardiovascular complications, including heart disease, are a leading cause of death for people with diabetes, who tend to suffer cardiovascular disease decades earlier than non-diabetics.

“Gaining weight may reflect good or better treatment with insulin therapy, which may partly explain why participants who gained weight over time had lower mortality rates,” said Trevor Orchard, M.D., professor of epidemiology at the University of Pittsburgh Graduate School of Public Health (GSPH), who is presenting the findings during the 67th annual meeting of the American Diabetes Association. Scientific sessions take place June 22-26 at the McCormick Place Convention Center, Chicago.

For this particular report, Dr. Orchard and his colleagues focused on 315 patients with type 1 diabetes participating in the Pittsburgh Epidemiology of Diabetes Complications Study, an 18-year prospective study of childhood onset type 1 diabetes, which began in 1986. As part of the study, the patients recently received a special computed tomography scan (CT) to assess coronary artery calcification.

The participants’ mean age was 42, and mean duration of diabetes was 34 years. In addition to the CT scan, patients were evaluated for fat underneath the skin and in the abdominal region, body mass index (BMI) and waist circumference. Although investigators noted a positive association for all measures of fatness and having any coronary artery calcification, in the two-thirds of patients who had calcification, the relationship reversed so that people with more fat had less severe calcification.

This association also varied by gender. Women with less fat under the skin had more evidence of coronary artery calcification than those with more fat. Thinner men also had more evidence of coronary artery calcification than men with a higher BMI.

“What it comes down to is a kind of double-edged relationship,” said Baqiyyah Conway, M.P.H., lead author of the abstract, adding that these associations of less severe artery calcification with greater fat persisted even when controlling for standard cardiovascular disease risk factors such as increased levels of LDL, or bad cholesterol, triglycerides, high blood pressure and lower levels of HDL, or good cholesterol. Controlling for kidney disease, another common complication of diabetes, weakened the association in men but not in women.

“This is not a firm recommendation to people with type 1 diabetes to put on weight, but it does raise the possibility that weight recommendations in type 1 diabetes may be somewhat different than those for the general population, and emphasizes the complex relationship between body fat and cardiovascular risk in diabetes,” said Dr. Orchard, who also is professor of medicine and pediatrics at the University of Pittsburgh School of Medicine.

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CONTACT: Amy Dugas, DugasAK@upmc.edu
PHONE: (412) 647-3555

EMBARGOED FOR RELEASE UNTIL 5 P.M., EDT, SATURDAY, JUNE 23

In addition to Dr. Orchard and Ms. Conway, other authors are Rachel G. Miller, M.S.; Tina Costacou, Ph.D.; and Daniel Edmundowicz, M.D., all of the University of Pittsburgh Schools of the Health Sciences.

Founded in 1948 and fully accredited by the Council on Education for Public Health, GSPH is world-renowned for contributions that have influenced public health practices and medical care for millions of people. One of the top-ranked schools of public health in the United States, GSPH was the first fully-accredited school of public health in the Commonwealth of Pennsylvania, with alumni who are among the leaders in their fields of public health. A member of the Association of Schools of Public Health, GSPH currently ranks third among schools of public health in NIH funding received. The only school of public health in the nation with a chair in minority health, GSPH is a leader in research related to women’s health, HIV/AIDS and human genetics, among others. For more information about GSPH, visit the GSPH Web site at http://www.publichealth.pitt.edu.

Note to editors: This presentation is abstract No. 0129-OR, scheduled for 5 p.m., EDT, Saturday, June 23.

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Largest ever study of genetics of common diseases published today

Contact: Craig Brierley
c.brierley@wellcome.ac.uk
44-207-611-7329
Wellcome Trust

The Wellcome Trust Case Control Consortium, the largest ever study of the genetics behind common diseases such as diabetes, rheumatoid arthritis and coronary heart disease, today publishes its results in the journals Nature and Nature Genetics.

The £9 million study is one of the UK’s largest and most successful academic collaborations to date. It has examined DNA samples from 17,000 people across the UK, bringing together 50 leading research groups and 200 scientists in the field of human genetics from dozens of UK institutions. Over two years, they have analysed almost 10 billion pieces of genetic information.

“Many of the most common diseases are very complex, part ‘nature’ and ‘nurture’, with genes interacting with our environment and lifestyles,” says Professor Peter Donnelly, Chair of the Consortium, who is based at the University of Oxford. “By identifying the genes underlying these conditions, our study should enable scientists to understand better how disease occurs, which people are most at risk and, in time, to produce more effective, more personalised treatments.”

The study has substantially increased the number of genes known to play a role in the development of some of our most common diseases. Many of these genes that have been found are in areas of the genome not previously thought to have been related to the diseases.

“Just a few years ago it would have been thought wildly optimistic that it would be possible in the near future to study a thousand genetic variants in each of a thousand people,” says Dr Mark Walport, Director of the Wellcome Trust, the UK’s largest medical research charity, which funded the study. “What has been achieved in this research is the analysis of half a million genetic variants in each of seventeen thousand individuals, with the discovery of more than ten genes that predispose to common diseases.

“This research shows that it is possible to analyse human variation in health and disease on an enormous scale. It shows the importance of studies such as the UK Biobank, which is seeking half a million volunteers aged between 40 and 69, with the aim of understanding the links between health, the environment and genetic variation. New preventive strategies and new treatments depend on a detailed understanding of the genetic, behavioural and environmental factors that conspire to cause disease.”

Amongst the most significant new findings are four chromosome regions containing genes that can predispose to type 1 diabetes and three new genes for Crohn’s disease (a type of inflammatory bowel disease). For the first time, the researchers have found a gene linking these two autoimmune diseases, known as PTPN2.

The study has also confirmed the importance of a process known as autophagy in the development of Crohn’s disease. Autophagy, or “self eating”, is responsible for clearing unwanted material, such as bacteria, from within cells. The may be key to the interaction of gut bacteria in health and in inflammatory bowel disease and could have clinical significance in the future.

“The link between type 1 diabetes and Crohn’s disease is one of the most exciting findings to come out of the Consortium,” says Professor John Todd from the University of Cambridge, who led the study into type 1 diabetes. “It is a promising avenue for us to understand how the two diseases occur. The pathways that lead to Crohn’s disease are increasingly well understood and we hope that progress in treating Crohn’s disease may give us clues on how to treat type 1 diabetes in the future.”

Research from the Consortium has already played a major part in identifying the clearest genetic link yet to obesity and three new genes linked to type 2 diabetes, published in April in advance of the main study. It has found independently a major gene region on chromosome 9 identified by independent studies on coronary heart disease.

Researchers analysed DNA samples taken from people in the UK – 2,000 patients for each disease and 3,000 control samples – to identify common genetic variations for seven major diseases. These are bipolar disorder, Crohn’s disease, coronary heart disease, hypertension, rheumatoid arthritis and type 1 and type 2 diabetes. For each disease, the researchers will study larger population samples to confirm their results.

Although the human genome is made up of more than three billion sub-units of DNA, called nucleotides (or bases), most of these show little in the way of differences between individuals. A substantial part of the variation in DNA sequence between individuals is due to single-nucleotide polymorphisms (differences), also known as SNPs. There are approximately 8 million common SNPs in European populations. Fortunately, because SNPs that lie close together on chromosomes often tell quite similar stories, researchers in the Consortium were able to explore this variation through analysing a subset of these SNPs (in fact approximately 500,000).

“Human genetics has a chequered history of irreproducible results, but this landmark collaboration of scientists in Britain has shown conclusively that the new approach of analysing a large subset of genetic variants in large samples of patients and healthy individuals works,” says Professor Donnelly. “We are now able to effectively scan most of the common variation in the human genome to look for variants associated with diseases. This approach will undoubtedly herald major advances in how we understand and tackle disease in the future.”

Further analysis as part of the Consortium will be looking at tuberculosis (TB), breast cancer, autoimmune thyroid disease, multiple sclerosis and ankylosing spondylitis. The results are expected later this year.

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The Wellcome Trust Case Control Consortium, the largest ever study of the genetics behind common diseases such as diabetes, rheumatoid arthritis and coronary heart disease publishes its results in the journals Nature and Nature Genetics.

The £9 million study is one of the UK’s largest and most successful academic collaborations to date. It has examined DNA samples from 17,000 people across the UK, bringing together 50 leading research groups and 200 scientists in the field of human genetics from dozens of UK institutions. Over two years, they have analysed almost 10 billion pieces of genetic information.

Researchers have uncovered genetic variations for seven major diseases: bipolar disorder, Crohn’s disease, coronary heart disease, hypertension, rheumatoid arthritis and type 1 and type 2 diabetes.

Speakers:

Dr Mark Walport – Director, Wellcome Trust

Professor Peter Donnelly (University of Oxford) – Chair, Wellcome Trust Case Control Consortium

Professor John Todd (University of Cambridge) – Type 1 diabetes

Dr Miles Parkes (Addenbrooke’s Hospital and University of Cambridge) – Crohn’s disease

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