BreakThrough Digest Medical News |
- Scientists discover how the brain ages
- A carefully scheduled high-fat diet resets metabolism and prevents obesity
- An important breakthrough in the fight against muscular dystrophies
- ‘Mad Cow’ blood test now on the horizon
| Scientists discover how the brain ages Posted: 11 Sep 2012 09:00 PM PDT The ageing process has its roots deep within the cells and molecules that make up our bodies. Experts have previously identified the molecular pathway that react to cell damage and stems the cell’s ability to divide, known as cell senescence.
However, in cells that do not have this ability to divide, such as neurons in the brain and elsewhere, little was understood of the ageing process. Now a team of scientists at Newcastle University, led by Professor Thomas von Zglinicki have shown that these cells follow the same pathway. This challenges previous assumptions on cell senescence and opens new areas to explore in terms of treatments for conditions such as dementia, motor neuron disease or age-related hearing loss. Newcastle University’s Professor Thomas von Zglinicki who led the research said: “We want to continue our work looking at the pathways in human brains as this study provides us with a new concept as to how damage can spread from the first affected area to the whole brain.” Working with the University’s special colony of aged mice, the scientists have discovered that ageing in neurons follows exactly the same rules as in senescing fibroblasts, the cells which divide in the skin to repair wounds. DNA damage responses essentially re-program senescent fibroblasts to produce and secrete a host of dangerous substances including oxygen free radicals or reactive oxygen species (ROS) and pro-inflammatory signalling molecules. This makes senescent cells the ‘rotten apple in a basket’ that can damage and spoil the intact cells in their neighbourhood. However, so far it was always thought that ageing in cells that can’t divide – post-mitotic, non-proliferating cells – like neurons would follow a completely different pathway. Now, this research explains that in fact ageing in neurons follows exactly the same rules as in senescing fibroblasts. Professor von Zglinicki, professor of Cellular Gerontology at Newcastle University said: “We will now need to find out whether the same mechanisms we detected in mouse brains are also associated with brain ageing and cognitive loss in humans. We might have opened up a short-cut towards understanding brain ageing, should that be the case.” Dr Diana Jurk, who did most of this work during her PhD in the von Zglinicki group, said: “It was absolutely fascinating to see how ageing processes that we always thought of as completely separate turned out to be identical. Suddenly so much disparate knowledge came together and made sense.” ### The research contributes to the Newcastle Initiative on Changing Age, the University’s response to the societal challenge of Ageing, seeking new ways to make the most of the extensive opportunities associated with increasing human longevity. The team want to further study the mechanism using the unique resource of the Newcastle Brain Bank. Contact: Karen Bidewell |
| A carefully scheduled high-fat diet resets metabolism and prevents obesity Posted: 11 Sep 2012 09:00 PM PDT New research from the Hebrew University of Jerusalem shows that a carefully scheduled high-fat diet can lead to a reduction in body weight and a unique metabolism in which ingested fats are not stored, but rather used for energy at times when no food is available.
The research was conducted by Prof. Oren Froy along with Prof. Zecharia Madar, research student Yoni Genzer and research fellow Dr. Hadas Sherman at the Institute of Biochemistry, Food Science and Nutrition, at the Hebrew University’s Robert H. Smith Faculty of Agriculture, Food and Environment. The results were published in FASEB Journal under the title ‘Timed high-fat diet resets circadian metabolism and prevents obesity.’ Previous research has established that disrupting mammals’ daily rhythms, or feeding them a high-fat diet, disrupts metabolism and leads to obesity. The researchers wanted to determine the effect of combining a high-fat diet with long-term feeding on a fixed schedule. They hypothesized that careful scheduling of meals would regulate the biological clock and reduce the effects of a high-fat diet that, under normal circumstances, would lead to obesity. For 18 weeks they fed a group of mice a high-fat diet on a fixed schedule (eating at the same time and for the same length of time every day). They compared these mice to three control groups: one that ate a low-fat diet on a fixed schedule, one that ate an unscheduled low-fat diet (in the quantity and frequency of its choosing), and one that ate an unscheduled high-fat diet. All four groups of mice gained weight throughout the experiment, with a ?nal body weight greater in the group that ate an unscheduled high-fat diet. The mice on the scheduled high-fat diet had a lower final body weight than the mice eating an unscheduled high-fat diet. But surprisingly, the mice on the scheduled high-fat diet also had a lower final body weight than the mice that ate an unscheduled low-fat diet, even though both groups consumed the same amount of calories. In addition, the mice on the scheduled high-fat diet exhibited a unique metabolic state in which the fats they ingested were not stored, but rather utilized for energy at times when no food was available, such as between meals. According to Prof. Froy, “Our research shows that the timing of food consumption takes precedence over the amount of fat in the diet, leading to improved metabolism and helping to prevent obesity. Improving metabolism through the careful scheduling of meals, without limiting the content of the daily menu, could be used as a therapeutic tool to prevent obesity in humans.” Contact: Dov Smith |
| An important breakthrough in the fight against muscular dystrophies Posted: 11 Sep 2012 09:00 PM PDT
An important breakthrough could help in the fight against myotonic dystrophy. The discovery, recently published in the prestigious scientific journal Cell, results from an international collaboration between researchers at the IRCM, the Massachusetts Institute of Technology (MIT), the University of Southern California and Illumina. Their findings could lead to a better understanding of the causes of this disease.
Myotonic dystrophy (DM), also known as Steinert’s disease, is the most common form of muscular dystrophies seen in adults. This disorder is characterized by muscle weakness and myotonia (difficulty in relaxing muscles following contraction). It is a multi-system disease, typically involving a wide range of tissues and muscle. “We studied a specific family of proteins called muscleblind-like proteins (Mbnl), which were first discovered in the fruit fly Drosophila melanogaster,” says Dr. Éric Lécuyer, Director of the RNA Biology research unit at the IRCM. “These RNA-binding proteins are known to play important functions in muscle and eye development, as well as in the pathogenesis of DM in humans.” Because of the extreme heterogeneity of clinical symptoms, DM has been described as one of the most variable and complicated disorders known in medicine. The systems affected, the severity of symptoms, and the age of onset of those symptoms greatly vary between individuals, even within the same family. “In patients with DM, levels of Mbnl proteins are depleted to different extents in various tissues,” explains Dr. Neal A.L. Cody, postdoctoral fellow in Dr. Lécuyer’s laboratory. “These alterations in levels and functions of Mbnl proteins are thought to play an important role in causing the disease.” “The global transcriptome analyses conducted in this study yielded several insights into Mbnl function and established genomic resources for future functional, modeling, and clinical studies,” add Drs. Christopher B. Burge and Eric T. Wang from MIT, the researchers who headed the study. “This knowledge will be invaluable in reconstructing the order of events that occur during DM pathogenesis, and could lead to the development of diagnostic tools for monitoring disease progression and response to therapy.” According to Muscular Dystrophy Canada, myotonic dystrophy is the most common form of muscle disease, affecting approximately one person in 8,000 worldwide. However, in Quebec’s region of Charlevoix / Saguenay-Lac-Saint-Jean, the prevalence is exceptionally high, with one person in 500 affected by the disease. There is no cure for myotonic dystrophy at the present time. Treatment is symptomatic, meaning that problems associated with myotonic dystrophy are treated individually. ### About the research project
This research project was funded by grants from the National Institutes of Health (NIH) to Christopher B. Burge and by an NIH training grant and a Muscular Dystrophy Foundation fellowship to Eric T. Wang. Work conducted by Neal A.L. Cody in Dr. Lécuyer’s laboratory was funded by the Fonds de Recherche du Québec ? Santé. The article published in Cell, Transcriptome-wide Regulation of Pre-mRNA Splicing and mRNA Localization by Muscleblind Proteins, was prepared by Eric T. Wang, Thomas T. Wang, Daniel J. Treacy, David E. Housman and Christopher B. Burge from the David K. Koch Institute for Integrative Cancer Research at the Massachusetts Institute of Technology (MIT); Neal A.L. Cody and Éric Lécuyer from the IRCM; Sonali Jog, Michela Biancolella and Sita Reddy from the University of Southern California; and Shujun Luo and Gary P. Schroth from Illumina Inc. For more information on this scientific breakthrough, please refer to the article summary published online by Cell: http://www.cell.com/abstract/S0092-8674(12)00885-9. About Dr. Éric Lécuyer
Éric Lécuyer obtained his PhD in molecular biology from the Université de Montréal. He is an Assistant IRCM Research Professor and Director of the RNA Biology research unit. Dr. Lécuyer is assistant professor-researcher in the Department of Biochemistry at the Université de Montréal. He is also adjunct professor in the Department of Medicine (Division of Experimental Medicine) at McGill University. Dr. Lécuyer is a research scholar from the Fonds de recherche du Québec ? Santé. For more information, visit www.ircm.qc.ca/lecuyer. About the IRCM
Founded in 1967, the Institut de recherches cliniques de Montréal (IRCM) (www.ircm.qc.ca) is currently comprised of 37 research units in various fields, namely immunity and viral infections, cardiovascular and metabolic diseases, cancer, neurobiology and development, systems biology and medicinal chemistry. It also houses three specialized research clinics, eight core facilities and three research platforms with state-of-the-art equipment. The IRCM employs 425 people and is an independent institution affiliated with the Université de Montréal. The IRCM clinic is associated to the Centre hospitalier de l’Université de Montréal (CHUM). The IRCM also maintains a long-standing association with McGill University. Contact: Julie Langelier |
| ‘Mad Cow’ blood test now on the horizon Posted: 10 Sep 2012 09:00 PM PDT Using newly available genetic sequencing scientists discovered cells infected with prions (the infectious agent responsible for these diseases) release particles which contain easily recognized ‘signature genes’.
Associate Professor Andrew Hill ? from the Department of Biochemistry and Molecular Biology at the Bio21 Institute ? said these particles travel in the blood stream, making a diagnostic blood test a possibility. “This might provide a way to screen people who have spent time in the UK, who currently face restrictions on their ability to donate blood,” he said. “With a simple blood test nurses could deem a prospective donor’s blood as healthy, with the potential to significantly boost critical blood stocks.” Mad Cow disease was linked to the deaths of nearly 200 people in Great Britain who consumed meat from infected animals in the late 1980s. Since 2000, the Australia Red Cross Blood Service has not accepted blood from anybody who lived in the UK for more than six months between 1980 and 1996, or who received a blood transfusion in the UK after 1980. The research is published in this week’s Oxford University Press Nucleic Acids Research journal ? http://nar.oxfordjournals.org/content/early/2012/09/08/nar.gks832.full. Lead author Dr Shayne Bellingham said the breakthrough might also help detect other human neurodegenerative diseases, such as Alzheimer’s and Parkinson’s. “This is an exciting new field where we can test for conditions in the brain and throughout the body, without being invasive,” he said. The researchers’ genetic testing focused on a form of cell discharge called exosomes. If exosomes were infected with prions (the pathogen that causes Creutzfeldt-Jakob Disease and Bovine Spongiform Encephalopathy, commonly known as Mad Cow Disease) they were found to also carry a specific signature of small genes called microRNA’s. ### The research was undertaken at the University of Melbourne, with assistance from the Mental Health Research Institute of Victoria, the National Health and Medical Research Council and the Australian Research Council. Contact: Associate Professor Andrew Hill |
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