“Exercise in a pill” is how scientists are describing a remarkable discovery where they used drugs to switch on genetic triggers that are normally only activated by exercise, to dramatically increase endurance in mice and confer other related benefits.

The study is published in the 31st July advanced online edition of Cell and is the work of researchers at the Salk Institute for Biological Studies, La Jolla, California, and other colleagues.

The discovery should help to develop treatments for muscle diseases and a range of metabolic disorders, including diabetes, and any athletes tempted to use the drugs, which are not commercially available, to boost performance in the coming Olympics can forget it since the lead researcher is already working with anti-doping officials to get a test for the drugs in place for this summer’s games, according to a statement from the Salk Institute.

Led by Howard Hughes Medical Investigator Dr Ronald M Evans, a professor in the Gene Expression Laboratory at the Salk Institute, the investigators found that triggering two signalling pathways with oral drugs turned laboratory mice into long-distance runners and appeared to confer other benefits of exercise.

Using genetic engineering, Evans and his team had already found that switching on a gene pathway called PPAR delta turned laboratory mice into marathon runners. Also, when fed a high fat diet that made other mice obese, the treated mice did not gain weight, and their response to insulin also improved, and reduced their blood sugar levels.

Evans said they wanted to find out if a drug could produce the same effect on PPAR delta, since genetic engineering (called genetic doping when referring to athletic performance), although feasible, was not a practical solution for humans.

They focused on an experimental drug called GW1516 that seemed to fit the bill and fed it to laboratory mice for four weeks. The drug is not available commercially. But they were surprised by the results, as lead author and postdoctoral researcher, Dr Vihang A Narkar explained:

“We got the expected benefits in lowering fatty acids and blood glucose levels but no effect, absolutely none, on exercise performance.”

So Narkar decided to try the next stage: would the drug show the desired effect if the mice were to have some exercise? So he had them run for up to 50 minutes every day on a treadmill.

This produced the desired effect; endurance in exercising mice treated with GW1516 went up by 77 per cent compared to exercising mice not on the drug. The drug also increased the proportion of “non-fatiguing” or “slow twitch”muscle fibres, said Narkar.

It would appear that GW1516 alone only boosted endurance and affected the muscle fibres when combined with some exercise. Narkar said they wondered if this was because of ATP, the chemical that delivers energy to muscles. When the body’s demand for energy is high, ATP releases all its energy and becomes AMP, and when AMP goes up, it triggers AMPK, a metabolic regulator that increases production of ATP. They wondered if perhaps PPAR delta only got involved once the AMPK switched on.

AMPK normally resides in the cytoplasm that surrounds the nucleus of each cell, but closer inspection revealed that in this experiment, some exercise-activated AMPK molecules had got into the nucleus, interacted with the PPAR delta and increased its effect on endurance.

“It essentially puts a turbo charge on PPAR delta, which explains why exercise is so important,” explained Evans.

So all that remained was to find a way to produce the same ATP-AMP effect without exercise. In a further experiment, the investigatos fed untrained mice a substance called AICAR, a synthetic vesion of AMP that triggers the AMPK switch directly.

After four weeks, with no training, the mice on synthetic AMP were able to run 44 per cent longer than untreated, untrained mice. Narkar said that was about the same improvement we can get with regular exercise.

The researchers concluded that:

” These results demonstrate that AMPK-PPAR delta pathway can be targeted by orally active drugs to enhance training adaptation or even to increase endurance without exercise.”

However, before the couch potatoes and aspiring Olympic contenders get tempted by the idea of taking “exercise in a pill”, they may wish to reflect on the fact that Evans is already working officials at the World Anti-Doping Association on a blood and urine test that detects AICAR, GW1516 and its metabolites.

“AMPK and PPARdelta Agonists Are Exercise Mimetics.”
Vihang A. Narkar, Michael Downes, Ruth T. Yu, Emi Embler, Yong-Xu Wang, Ester Banayo, Maria M. Mihaylova, Michael C. Nelson, Yuhua Zou, Henry Juguilon, Heonjoong Kang, Reuben J. Shaw, and Ronald M. Evans.
Cell Advance online edition 31 July 2008
DOI: 10.1016/j.cell.2008.06.051

Click here for Abstract.

Sources: Salk Institute, journal abstract.

Written by: Catharine Paddock, PhD
Copyright: Medical News Today

People with schizophrenia bear an “increased burden” of rare deletions and duplications of genetic material, genome-wide, say researchers supported in part by the National Institute of Mental Health (NIMH), a component of the National Institutes of Health (NIH).

“Although many of us have these changes in our genetic material, they are about 15 percent more frequent in people with schizophrenia,” explained Pamela Sklar, M.D., Ph.D., of Harvard University and the Stanley Center for Psychiatric Research. “We also discovered two large areas of chromosomal deletions that confer a great deal of risk for schizophrenia and confirm involvement of a third previously reported area.”

Sklar and colleagues in the International Schizophrenia Consortium team, representing 11 research institutes worldwide, report on the largest study of its kind to date, online July 30, 2008, in the journal .

“By implicating two previously unknown sites, this study triples the number of genomic areas definitely linked to schizophrenia,” said NIMH Director R Thomas Insel, M.D. “It also confirms in a large sample that unraveling the secrets of rare structural genetic variation may hold promise for improved diagnosis, treatment and prevention of such neuro-developmental disorders.”

Although recent smaller studies had identified such structural genetic glitches in schizophrenia, this genome-wide association study is the first large enough to detect weak signals that might otherwise be drowned out amid a din of statistical noise. Genetic factors are thought to account for 73 to 90 percent of schizophrenia, but most of these have so far eluded detection.

In search of rare illness-linked genetic variations, Sklar and colleagues scanned the genomes of 3,391 schizophrenia cases and 3,181 controls in a European sample.

The cases showed a subtle, but statistically significant increased number of such variations, which were found in 13.1 percent of cases and 10.4 percent of controls. Variations affected 1.41-fold more genes in people with schizophrenia, who also had a 1.45-fold higher prevalence of the rarest glitches - those that occurred only once.

The large sample also allowed the researchers to pinpoint previously undiscovered chromosomal locations associated with schizophrenia. An area on Chromosome 15 harbored deletions in 9 cases and no controls, while an area on Chromosome 1 had deletions in 10 cases and only one control.

“This tells us that variations in both of these areas are very potent risk factors for schizophrenia,” said Sklar.

The researchers also confirmed in 13 cases a previously-reported association between schizophrenia and a deletion on chromosome 22 known to cause velo-cardio-facial syndrome. Other suspect sites identified were on Chromosomes 12 and 16 and in genes relevant to neural development and growth.

Exactly how the subtly increased number of structural variations in schizophrenia might translate into illness remains to be discovered, say the researchers.

The same sites of deletions on Chromosomes 1 and 15 reported by Sklar and colleagues, as well as an additional area on Chromosome 15, are also implicated in schizophrenia by another large study published online the same day in Nature by another international group of researchers supported in part by NIMH.

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The International Schizophrenia Consortium is composed of researchers at: Cardiff University, Karolinska Institute/University of North Carolina at Chapel Hill, Trinity College Dublin, University College London, University of Aberdeen, University of Edinburgh, Queensland Institute of Medical Research, University of Southern California, Massachusetts General Hospital, Stanley Center for Psychiatric Research and Broad Institute of MIT and Harvard.

References:

The International Schizophrenia Consortium. Rare chromosomal deletions and duplications increase risk of schizophrenia. Nature. 2008 Jul 30, online.

Stefansson h, et al. Large recurrent microdeletions associated with schizophrenia. Nature. 2008 Jul 30, online.

The National Institute of Mental Health (NIMH) mission is to reduce the burden of mental and behavioral disorders through research on mind, brain, and behavior. More information is available at the NIMH website, http://www.nimh.nih.gov/.

The National Institutes of Health (NIH) - The Nation’s Medical Research Agency - includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit http://www.nih.gov/.

Source: Jules Asher
NIH/National Institute of Mental Health

Thermo Fisher Scientific Inc., the world leader in serving science, will exhibit a new spectrophotometer that offers unique benefits for human leukocyte antigen (HLA) typing laboratories dealing with donor tissue matching. The Thermo Scientific NanoDrop™ 1000 represents the growing trend of successful genome research tools finding their way to the clinical research setting. Specifically, the NanoDrop 1000 is utilized in the workflow as a replacement to time-consuming traditional spectrophotometers where efficiency and time-to-result are critical.

The NanoDrop 1000 is capable of carrying out full UV-Vis absorbance measurements with only 1 ul of undiluted sample, enabling HLA laboratories to significantly speed up analysis time. The NanoDrop 1000 has been integrated into tissue typing workflows through a validation process as set by the HLA typing community. The NanoDrop 1000 spectrophotometer will be showcased for the first time at the Thermo Scientific booth 2739 at AACC 2008, being held in Washington D.C., from July 29 - 31.

This innovative cuvetteless method enables HLA laboratories to quickly and effectively process DNA samples without compromising yield. HLA is the major histocompatibility complex in humans, and laboratories performing HLA typing have distinct requirements for instrumentation, including preserving sample yield and optimizing analysis time. The NanoDrop 1000 spectrophotometer has been successfully integrated into the HLA typing workflow in a number of leading laboratories. DNA is extracted and purified from donor tissue and quantified on the NanoDrop 1000 using a patented sample retention system requiring only 1 ul of sample. This quantitation method enables HLA laboratories to quickly and effectively process DNA samples without compromising yield.

In many HLA cases, donor workup results are required in less than four hours as the speed and accuracy of tissue analysis can affect the long-term graft survival of the tissue. The NanoDrop 1000 spectrophotometer allows laboratories to analyze microsamples of DNA in only 10 seconds, reducing labor time and increasing laboratory productivity. Additionally, the novel microsample quantitation technology of the NanoDrop 1000 is critical for typing samples of limited cell mass, such as mononucleated bone marrow specimens.

In addition to reducing spectrophotometric quantitation prior to DNA amplification, the NanoDrop 1000 enables HLA typing laboratories to comply with the strict standards set by the ASHI. The NanoDrop 1000 has passed the rigorous validation process for HLA laboratories across the United States, and is now recommended by many certified laboratory inspectors.

Notes

For more information about the Thermo Scientific NanoDrop 1000 spectrophotometer, please visit the Thermo Scientific booth 2739 at AACC 2008. Alternatively please email nanodrop@thermofisher.com, call +1 302-479-7707 or visit http://www.nanodrop.com.

Spectrophotometers are general purpose laboratory instruments. They have not been cleared or approved by the United States Food and Drug Administration, the European IVD Directive or any other agency for diagnostic, clinical or other medical use.

Thermo Scientific is part of Thermo Fisher Scientific Inc. the world leader in serving science.

About Thermo Fisher Scientific

Thermo Fisher Scientific Inc. (NYSE: TMO) is the world leader in serving science, enabling our customers to make the world healthier, cleaner and safer. With annual revenues of $10 billion, we have more than 30,000 employees and serve over 350,000 customers within pharmaceutical and biotech companies, hospitals and clinical diagnostic labs, universities, research institutions and government agencies, as well as environmental and industrial process control settings. Serving customers through two premier brands, Thermo Scientific and Fisher Scientific, we help solve analytical challenges from routine testing to complex research and discovery. Thermo Scientific offers customers a complete range of high-end analytical instruments as well as laboratory equipment, software, services, consumables and reagents to enable integrated laboratory workflow solutions. Fisher Scientific provides a complete portfolio of laboratory equipment, chemicals, supplies and services used in healthcare, scientific research, safety and education. Together, we offer the most convenient purchasing options to customers and continuously advance our technologies to accelerate the pace of scientific discovery, enhance value for customers and fuel growth for shareholders and employees alike.

Thermo Fisher Scientific

Two international teams of scientists working on independent studies have discovered that rare deletions and duplications in genetic material appear to occur in greater numbers in people who have schizophrenia.

The studies are published in the July 30th online issue of the journal Nature. One study is by the International Schizophrenia Consortium (ISC), a team of researchers from 12 institutions in Europe, the United States and Australia, and the other is by SGENE consortium, a team of researchers from 18 institutions across Europe, the United States and China.

1 in every 100 people is affected by schizophrenia at some point in their lives. It is a serious mental illness and around 70 per cent of cases are thought to have a genetic basis. However, like many psychatric disorders, it is not linked to one gene, but several, making it difficult to pin down.

Between them the two studies, which were essentially surveys that trawled the human genome, found that people missing certain sections of genetic material had up to 15 times the risk of developing schizophrenia compared to the general population.

The ISC researchers looked for a particular type of genetic error in 3,391 schizophrenia patients. The type of genetic error they investigated is called a copy number variation, where a particular section of genome is either missing or duplicated.

The SGENE researchers catalogued copy number variations between 15,000 parents and their children and then looked for them in two groups of schizophrenia patients, one with 1,433 people and the other with 3,285 people.

Both the ISC and the SGENE researchers found the same three copy number variations were linked to schizophrenia: one on chromosome 1, another on chromosome 15 and a third on chromosome 22. The one on chromosome 22 had alread been linked to schizophrenia before.

The SGENE team also found an extra copy number variation on chromosome 15, while the ISC team found that people with schizophrenia were more likely to have rare copy number variations than people who did not have the disease.

The frequency of these rare variations in the population at large is thought to be about 1 per cent, but the teams were not too sure about that. The risk of developing schizophrenia was estimated to be between 3 and 15 times greater than the general population for persons who had rare copy number variations, depending on the combination of deletions and duplications.

Understanding the genetics of schizophrenia and similar disorders relies heavily on large collaborative studies, because the variations are so rare. Kári Stefánsson, chief executive of Iceland based deCODE genetics, a member of the SGENE collaboration, said:

“We may have to identify a larger number of rare but high-risk variants to understand the genetic contribution to susceptibility.”

The coincidence of findings between the two independent groups, each using a different approach, has been welcomed by experts as an important step in understanding the genetic basis of schizophrenia, although there is still some way to go before the picture can be described as complete.

A member of the ISC team, Pamela Sklar of Harvard Medical School in Cambridge, Massachusetts, said the fact the two studies approached the problem from different angles using different methodologies was “fantastic for psychiatric genetics”.

Speaking about the ISC study in particular, R Thomas Insel, Director of the National Institutes for Mental Health in the US, said that by finding two previously unknown sites, the researchers tripled the number of genomic areas linked to schizophrenia:

“It also confirms in a large sample that unraveling the secrets of rare structural genetic variation may hold promise for improved diagnosis, treatment and prevention of such neuro-developmental disorders,” he added.

Meanwhile, Jonathan Flint from the Wellcome Trust Centre for Human Genetics at the University of Oxford, UK, said it was not going to be easy to convert these findings into a better understanding of the biology of schizophrenia.

However, this is the first time that studies involving large populations have shown links between the genetic deletions and duplications and schizonphrenia, which Stefánsson described as a “first component to a molecular test to aid in clinical diagnosis and intervention”.

Marjorie Wallace, chief executive of the UK mental-health charity SANE, said there was good reason to be cautious, because “for years we have seen many false positives in the search for the gene or genes”, and although the results were encouraging, “they are a long way from finding the causes, treatment and, above all, much needed prevention of psychotic illness.” However, she emphasized the importance of continuing this kind of research because:

“It is very important to find out who is at risk [of schizophrenia] so they can avoid triggers such as cannabis.”

“Large recurrent microdeletions associated with schizophrenia.”
Hreinn Stefansson, Dan Rujescu, Sven Cichon, et al.
Nature Advance online publication, 30 July 2008.
doi:10.1038/nature07229

Click here for Abstract.

“Rare chromosomal deletions and duplications increase risk of schizophrenia.”
The International Schizophrenia Consortium.
Nature advance online publication, 30 July 2008.
doi:10.1038/nature07239

Click here for Abstract.

Sources: Nature News, NIMH.

Written by: Catharine Paddock, PhD
Copyright: Medical News Today

The race to ensure that scientists stop drug-taking athletes from damaging sport by using performance enhancing drugs or undergoing genetic manipulation is a constant challenge, according to a major four-decade review by three of the World’s leading experts on doping in sport.

Writing in the August issue of the European-based Journal of Internal Medicine, they say that significant advances have been made in the fight against drugs in sport over the last 40 years. However, the authorities face a constant battle to keep up with both the athletes who use drugs and their rogue scientific advisors.

“A cardinal feature of doping is that some athletes will experiment with any new substance that might improve their performance” says Professor Don Catlin, Founder and former Director of the World Anti-Doping Agency (WADA) accredited laboratory at the University of California, USA, and CEO of the Anti-Doping Research Institute.

“They do not wait for regulatory approvals. If they can obtain a supply they will try it. This means that scientists need to anticipate and develop tests even before the drug has been misused by athletes. “Considerable concerns have also been expressed about gene doping, a prohibited spin off of gene manipulation, a medical advance that has been developed to alter a person’s DNA to fight diseases like muscular dystrophy and cystic fibrosis.”

The paper is co-written with two other leading experts - Professor Arne Ljungqvist, Vice President of WADA and Professor Emeritus at the Karolinska Institute, Sweden, and Professor Ken Fitch from the University of Western Australia, who was a sports medicine consultant for the 2000 Olympic Games in Sydney.

Published to coincide with the Olympics, from 8 to 24 August, the review provides a highly authoritative view of sports doping over the last 40 years and looks at the challenges scientists may face in the future.

Even tougher doping control measures will be in force at this summer’s Games, according to Professor Ljungqvist, who is also Chairman of the International Olympic Committee’s Medical Commission. He points out that an estimated 4,500 samples will be collected from the 10,500 athletes taking part, considerably higher than the 2004 games in Athens.

Doping in sport first hit the headlines when a Danish cyclist died during the Rome Olympic Games in 1960. Cyclists had been taking strong stimulants since the late 19th century but up until then the sports authorities had failed to take action.

A Medical Commission was created by the International Olympic Committee to tackle the problem and various other sporting bodies followed suit. This culminated in the formation of WADA in 1999, where Professor Ljungqvist, as Chairman of its Health, Medical and Research Committee, played a pivotal role in developing the science needed to combat doping in sport.

“Remarkable advances have been made over the last 40 years which have allowed sports authorities to identify and sanction athletes who have misused a wide range of drugs, most of which were developed to treat diseases” says Professor Ljungqvist.

“More recently drugs have been produced and used to specifically enhance athletic performance and avoid detection. “At the same time strict regulations have been developed to ensure that athletes with a proven clinical need can still receive the prescription drugs they need without fear of sanctions.”

“This major review by Professors Catlin, Ljungqvist and Fitch provides a concise description of the history of drug testing for the Olympic Games, with fascinating details on the evolution of laboratory equipment and analytical strategies” says Dr Thomas H Murray, President and CEO of The Hastings Center, a bioethics research institute based in New York.

“It identifies failings of the overall anti-doping system - most of them out of the laboratories control - and describes a number of challenges to be confronted. “And it also shows us that there are five elements that are necessary for a successful anti-doping programme. These are: a strong commitment to - and sufficient funding for - research, a smart sampling strategy, adequate analytical capacity, a trustworthy adjudication process and a solid foundation of clear principles and transparent process.”

In his commentary on the paper, Dr Murray points out that research carried out at The Hastings Center suggests that the very competitiveness of sport has given doping great coercive power and that athletes would prefer a drug-free, level playing field.

And he agrees with the authors that scientists face a constant race to stay ahead of sports doping and pre-empt future trends.

“New scientific developments such as genetic manipulation demand an anti-doping system that is scientifically sophisticated, robust and capable of swift response” he maintains.

“An important part of that strategy is raising awareness of the problem and keeping the debate alive, which is why this paper in the Journal of Internal Medicine - written by three leading experts in the field - is so important.”

Notes

- Paper: Medicine and sport in the fight against doping in sport.
Catlin D H, Fitch K D andLjungqvist A.
Journal of Internal Medicine. 264, pp 99-114 (August 2008).

- Commentary: Doping in sport: challenges for medicine, science and ethics.Journal ofInternal Medicine. 264, pp 95-98. (August 2008).

- The Journal of Internal Medicine publishes original clinical work within the broad field of general and internal medicine and its sub-specialties, featuring original articles, reviews, and case reports. The journal also supports and organises scientific meetings (symposia) within the scope of the journal. http://www.blackwellpublishing.com/jim

About Wiley-Blackwell

Wiley-Blackwell was formed in February 2007 as a result of the acquisition of Blackwell Publishing Ltd. by John Wiley & Sons, Inc., and its merger with Wiley’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 1,400 scholarly peer-reviewed journals and an extensive collection of books with global appeal.

Wiley-Blackwell

Gene silencing techniques and induced pluripotent stem cell technology are among the cutting-edge approaches to Parkinson’s drug development funded through The Michael J. Fox Foundation’s Rapid Response Innovation Awards 2008. As part of its mission to drive transformative treatments and a cure for PD, the Foundation has awarded $1.1 million for 15 high-risk, high-reward Parkinson’s disease research projects under the initiative in the first half of the year. Applications are still being accepted, and a total of $2 million in Rapid Response awards is expected by year’s end.

Rapid Response helps keep new and novel approaches to Parkinson’s disease flowing into the drug development pipeline by allowing researchers to pursue their most exciting ideas in real time. The Foundation accepts Rapid Response proposals on a rolling basis with no deadline, and funding decisions are made within six weeks of application. Awards of up to $75,000 are available for one-year basic, preclinical or clinical research projects in any Parkinson’s-relevant arena. The program has met with an enthusiastic response from the research community, both within Parkinson’s disease and beyond, since it was first launched in January 2007.

“Rapid Response infuses capital quickly into exciting new ideas that could open up important new avenues of inquiry for Parkinson’s disease,” said Katie Hood, CEO of The Michael J. Fox Foundation. “Our goal is to provide the funding needed to further ‘build the case’ for these new concepts, developing the data required before other traditional funding sources can step in.”

The program’s application process and funding criteria emphasize speed and novelty. Funded projects typically are strong ideas being tested for the first time. Unlike other Foundation initiatives, Rapid Response allows for the submission of applications at any time of year. There is no pre-proposal triage stage, and the standard MJFF application has been shortened to three pages. Additionally, postdoctoral researchers are permitted to apply as principal investigators provided the head of their lab serves as administrative PI.

Among the potentially high-impact Rapid Response projects funded so far this year:

• Asa Abeliovich, MD, PhD, of Columbia University is working to determine whether a gene silencing technique using microRNAs - short, noncoding molecules of RNA - can be effective in reducing alpha-synuclein, a protein whose aggregation, or clumping, in the brain is a hallmark of Parkinson’s pathology.

• Jian Feng, PhD, of SUNY-Buffalo, and Patrick Alfryn Lewis, PhD, of the Institute of Neurology (London, UK) and John A. Hardy, PhD, University College London (London, UK) are conducting two separate investigations using newly discovered induced pluripotent stem cell (iPS) technology to shed greater light on the Parkinson’s-implicated genes parkin and LRRK2. Using iPS, the teams are engineering stem cells from skin cells, then using these engineered stem cells to generate human dopamine neurons with or without mutations in the respective genes. Both projects seek to characterize disease mechanisms set off by genetic mutations and to create new models for testing therapeutic approaches that could prevent these events from occurring.
• Rahul Srinivasan, MBBS, PhD, and Henry A. Lester, PhD, of the California Institute of Technology are working to better understand epidemiological findings that have consistently shown smoking may protect against PD. The researchers hope to elucidate the mechanisms by which nicotine may protect dopamine neurons through development and validation of a screening test for small molecules that could increase nicotine receptor expression in the brain.
• Marcus Unger, MD, and Wolfgang Oertel, MD, of Phillips University (Marburg, Germany) want to find better treatments for the digestive problems that dramatically affect Parkinson’s patients’ quality of life, as well as test the Braak hypothesis, which posits that Parkinson’s disease progresses through the body and to the brain in a series of stages starting in the gastrointestinal system. They are examining a possible link between constipation and Lewy body pathology in the gastric lining of people with PD.

Founded in 2000, The Michael J. Fox Foundation for Parkinson’s Research is dedicated to ensuring the development of a cure for Parkinson’s disease within the coming decade through an aggressively funded research agenda. The Foundation has funded $126 million in research to date.

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Source: Holly Barkhymer
The Michael J. Fox Foundation for Parkinson’s Research

National charity, Heart Research UK, has commented that the recent headline claiming an ‘obesity gene’ causes people to put on weight by keeping them hungry, is only a small factor into why people are overweight and shouldn’t be used as an excuse for them to accept their size.

Barbara Harpham, National Director of Heart Research UK, says: “This information is a useful thing to know but it is an explanation, not a reason. Findings like these can give those who are prone to being overweight an excuse to accept their size and not do anything about it. What they have to remember is that, behind the headline, this is only a small factor in why people are overweight - they have to make the right choices.”

The research, carried out by the University College of London, said that “Usually the act of eating “switches off” the appetite and creates a feeling of satiety or “fullness”, but the FTO gene stops this from happening.” On the other hand, Heart Research UK say that, although a percentage of the public may have this gene, it should not deter them from eating a healthy balanced diet and taking regular exercise which will become second nature within time. They also emphasised how important it is that people are given lifestyle advice and encouraged to make healthy lifestyle choices.

Notes

Heart Research UK is a visionary charity founded in 1967 by Mr Watson, a working heart surgeon, who realised that patients were dying unnecessarily because of the lack of research in heart disease, especially surgical techniques. Having funded six of the first eight UK heart transplants the charity leads the way funding ground breaking, medical research projects into the prevention, treatment and cure of heart disease. There is a strong emphasis on supporting clinical and surgical projects and young researchers on their first steps into research. The Charity currently funds over ￡2.5m of research projects at 33 hospitals and universities across the UK. In addition over ￡340,000 has been awarded to community-based lifestyle projects that aim to prevent or reduce the risks of heart disease.

Heart Research UK

Some of the biggest names in 20th century evolutionary biology such as Ernst Mayr and A.J. Cain considered that eastern Australian parrots of the Crimson Rosella Platycercus elegans group exemplified the phenomenon of ring speciation whereby reproductive isolation develops despite gene flow.

Using powerful tools of modern molecular genetics, the authors show that things are not always as they seem and that these birds still hold surprises.

Indeed, the molecular data suggest that complex patterns of selection and genetic drift coupled with Pleistocene landscape changes impacting the birds’ geographical range are needed to understand the group’s history.

Proceedings of the Royal Society B: Biological Sciences

Proceedings B is the Royal Society’s flagship biological research journal, dedicated to the rapid publication and broad dissemination of high-quality research papers, reviews and comment and reply papers. The scope of journal is diverse and is especially strong in organismal biology.

Proceedings of the Royal Society B: Biological Sciences

Recently in sponges several genes have been discovered controlling growth. Surprisingly many of these genes are also involved in developmental processes in humans.

For example a gene involved in patterning the nervous system in humans is closely related to one of the genes shaping the sponge.

We present a simulation model where a network of genes and the supply of nutrients from the environment is controlling growth and from of a sponge.

We demonstrate that we can approximate the growth form of a sponge and predict growth patterns.

Proceedings of the Royal Society B: Biological Sciences

Proceedings B is the Royal Society’s flagship biological research journal, dedicated to the rapid publication and broad dissemination of high-quality research papers, reviews and comment and reply papers. The scope of journal is diverse and is especially strong in organismal biology.

Proceedings of the Royal Society B: Biological Sciences

Breakthrough genetic research to map all the genes connected to Alzheimer’s, which could lead to more aggressive treatment and a potential cure for the disease, was the focus of a presentation by leading Alzheimer’s researcher Dr. Rudolph Tanzi at the International Conference on Alzheimer’s Disease (ICAD) in Chicago.

Tanzi, Chairman of the Cure Alzheimer’s Fund Research Consortium and the Joseph and Rose Kennedy Professor of Neurology at Harvard Medical School, was one of eight featured speakers discussing the genetic factors of Alzheimer’s disease as part of ICAD. Tanzi discussed his work on the “Alzheimer’s Genome Project” (AGP), identifying all of the genes that work individually or together to influence one’s risk of Alzheimer’s disease. A paper on AGP is currently under peer review at a prestigious science journal.

“With the innovative developments in genetic technology, completion of the human genome project and the advances in statistical analyses, we are on the cusp of a rare ’science moment’ that should greatly accelerate our efforts to treat and prevent Alzheimer’s disease,” Dr. Tanzi told conference attendees. “Every new Alzheimer’s gene we identify provides clues to the cause of this dreadful disease. The knowledge gained from the Alzheimer’s-associated defects in these genes should guide the development of novel therapeutics.”

Tanzi highlighted two specific areas of the AGP, funded by the Cure Alzheimer’s Fund. The genome-wide association screen is the largest such family-based screen ever conducted. Tanzi and his team collected genetic data from more than 1,300 families affected by Alzheimer’s disease to determine gene variants that influence one’s lifetime risk of Alzheimer’s. His presentation will cover a ‘novel’ gene, one of the top genetic hits for Alzheimer’s emerging from that screen.

In addition, Tanzi discussed AlzGene, a publicly available web database (http://alzgene.org) for researchers working to uncover the genetic underpinnings of Alzheimer’s disease. Spearheaded by Dr. Tanzi’s colleague, Lars Bertram, Assistant Professor of Neurology at MGH, AlzGene provides a comprehensive and systematic display of all published Alzheimer’s genetics research over the past 30 years. In addition, through analysis of the collective genetic data, Tanzi and Bertram have determined 30 genes that increase one’s lifetime risk for Alzheimer’s as well as others that protect against it. Their overarching goal is to combine the results of the AlzGene project and the genome-wide association screen to ultimately identify all the genes that significantly influence one’s lifetime genetic risk for Alzheimer’s disease. The first set of breakthroughs in this project will be presented by Dr. Tanzi at ICAD.

“Research findings in the past year alone have generated tremendous excitement in the field of neuroscience, genetics and especially in Alzheimer’s research,” said Tanzi. “Ultimately, the combined results of the family-based genome-wide screen and AlzGene should allow for the reliable prediction of Alzheimer’s disease while also guiding the development of novel therapies. These studies will someday lead to the development of therapies aimed at treating and preventing Alzheimer’s according to one’s personal genome.”

Cure Alzheimer’s Fund™ is a 501c3 public charity established to fund targeted research with the highest probability of slowing, stopping or reversing Alzheimer’s disease.

Cure Alzheimer’s Fund