BreakThrough Digest Medical News |
- Bees can ‘turn back time,’ reverse brain aging
- Epigenetics alters genes in rheumatoid arthritis
- Researchers report success in treating autism spectrum disorder
| Bees can ‘turn back time,’ reverse brain aging Posted: 02 Jul 2012 09:00 PM PDT Scientists at Arizona State University have discovered that older honey bees effectively reverse brain aging when they take on nest responsibilities typically handled by much younger bees. While current research on human age-related dementia focuses on potential new drug treatments, researchers say these findings suggest that social interventions may be used to slow or treat age-related dementia.
In a study published in the scientific journal Experimental Gerontology, a team of scientists from ASU and the Norwegian University of Life Sciences, led by Gro Amdam, an associate professor in ASU’s School of Life Sciences, presented findings that show that tricking older, foraging bees into doing social tasks inside the nest causes changes in the molecular structure of their brains. “We knew from previous research that when bees stay in the nest and take care of larvae ? the bee babies ? they remain mentally competent for as long as we observe them,” said Amdam. “However, after a period of nursing, bees fly out gathering food and begin aging very quickly. After just two weeks, foraging bees have worn wings, hairless bodies, and more importantly, lose brain function ? basically measured as the ability to learn new things. We wanted to find out if there was plasticity in this aging pattern so we asked the question, ‘What would happen if we asked the foraging bees to take care of larval babies again?” During experiments, scientists removed all of the younger nurse bees from the nest – leaving only the queen and babies. When the older, foraging bees returned to the nest, activity diminished for several days. Then, some of the old bees returned to searching for food, while others cared for the nest and larvae. Researchers discovered that after 10 days, about 50 percent of the older bees caring for the nest and larvae had significantly improved their ability to learn new things. Amdam’s international team not only saw a recovery in the bees’ ability to learn, they discovered a change in proteins in the bees’ brains. When comparing the brains of the bees that improved relative to those that did not, two proteins noticeably changed. They found Prx6, a protein also found in humans that can help protect against dementia ? including diseases such as Alzheimer’s ? and they discovered a second and documented “chaperone” protein that protects other proteins from being damaged when brain or other tissues are exposed to cell-level stress. In general, researchers are interested in creating a drug that could help people maintain brain function, yet they may be facing up to 30 years of basic research and trials. “Maybe social interventions ? changing how you deal with your surroundings ? is something we can do today to help our brains stay younger,” said Amdam. “Since the proteins being researched in people are the same proteins bees have, these proteins may be able to spontaneously respond to specific social experiences.” Amdam suggests further studies are needed on mammals such as rats in order investigate whether the same molecular changes that the bees experience might be socially inducible in people. Contact: Sandra Leander ### |
| Epigenetics alters genes in rheumatoid arthritis Posted: 03 Jul 2012 01:00 AM PDT Contact: Debra Kain It’s not just our DNA that makes us susceptible to disease and influences its impact and outcome. Scientists are beginning to realize more and more that important changes in genes that are unrelated to changes in the DNA sequence itself ? a field of study known as epigenetics ? are equally influential. A research team at the University of California, San Diego ? led by Gary S. Firestein, professor in the Division of Rheumatology, Allergy and Immunology at UC San Diego School of Medicine ? investigated a mechanism usually implicated in cancer and in fetal development, called DNA methylation, in the progression of rheumatoid arthritis (RA). They found that epigenetic changes due to methylation play a key role in altering genes that could potentially contribute to inflammation and joint damage. Their study is currently published in the online edition of the Annals of the Rheumatic Diseases. “Genomics has rapidly advanced our understanding of susceptibility and severity of rheumatoid arthritis,” said Firestein. “While many genetic associations have been described in this disease, we also know that if one identical twin develops RA that the other twin only has a 12 to 15 percent chance of also getting the disease. This suggests that other factors are at play ? epigenetic influences.” DNA methylation is one example of epigenetic change, in which a strand of DNA is modified after it is duplicated by adding a methyl to any cytosine molecule (C) ? one of the 4 main bases of DNA. This is one of the methods used to regulate gene expression, and is often abnormal in cancers and plays a role in organ development. While DNA methylation of individual genes has been explored in autoimmune diseases, this study represents a genome-wide evaluation of the process in fibroblast-like synoviocytes (FLS), isolated from the site of the disease in RA. FLS are cells that interact with the immune cells in RA, an inflammatory disease in the joints that damages cartilage, bone and soft tissues of the joint. In this study, scientists isolated and evaluated genomic DNA from 28 cell lines. They looked at DNA methylation patterns in RA FLS and compared them with FLS derived from normal individuals or patients with non-inflammatory joint disease. The data showed that the FLS in RA display a DNA methylome signature that distinguishes them from osteoarthritis and normal FLS. These FLS possess differentially methylated (DM) genes that are critical to cell trafficking, inflammation and cell?extracellular matrix interactions. “We found that hypomethylation of individual genes was associated with increased gene expression and occurred in multiple pathways critical to inflammatory responses,” said Firestein, adding that this led to their conclusion: Differentially methylated genes can alter FLS gene expression and contribute to the pathogenesis of RA.
### Additional contributors include Kazuhisa Nakano and David L. Boyle, UCSD Department of Medicine; and John W. Whitaker and Wei Wang, UCSD Department of Chemistry and Biochemistry. This project was supported by grant number UL1RR031980 from the National Institutes of Health’s National Center for Advancing Translational Science. NexDx, Inc. licensed the technology from UC San Diego and provided informatics support for this study. Gary S. Firestein and Wei Wang are on the Scientific Advisory Board of NexDx, Inc. |
| Researchers report success in treating autism spectrum disorder Posted: 01 Jul 2012 09:00 PM PDT
Using a mouse model of autism, researchers at the University of Cincinnati (UC) and Cincinnati Children’s Hospital Medical Center have successfully treated an autism spectrum disorder characterized by severe cognitive impairment.
The research team, led by Joe Clark, PhD, a professor of neurology at UC, reports its findings online July 2, 2012, in the Journal of Clinical Investigation, a publication of the American Society for Clinical Investigation. The disorder, creatine transporter deficiency (CTD) is caused by a mutation in the creatine transporter protein that results in deficient energy metabolism in the brain. Linked to the X chromosome, CTD affects boys most severely; women are carriers and pass it on to their sons. The brains of boys with CTD do not function normally, resulting in severe speech deficits, developmental delay, seizures and profound mental retardation. CTD is estimated to currently affect about 50,000 boys in the United States and is the second-most common cause of X-linked mental retardation after Fragile X syndrome. Following CTD’s discovery at UC in 2000, researchers at UC and Cincinnati Children’s led by Clark discovered a method to treat it with cyclocreatine?also known as CincY, and pronounced cinci-why?a creatine analogue originally developed as an adjunct to cancer treatment. They then treated genetically engineered mice as an animal model of the human disease. “CincY successfully entered the brain and reversed the mental retardation-like symptoms in the mice, with benefits seen in nine weeks of treatment,” says Clark, adding that no harmful effects to the mice were observed in the study. “Treated mice exhibited a profound improvement in cognitive abilities, including recognition of novel objects, spatial learning and memory.” As a repurposed drug (originally developed for another therapy), CincY has already been through part of the U.S. Food and Drug Administration (FDA) approval process. It is taken orally as a pill or powder. UC’s Office of Entrepreneurial Affairs and Technology Commercialization has reached agreement with Lumos Pharma, a privately held Austin, Texas, startup company based on UC technology, to develop and commercialize CincY. Lumos Pharma was created with technology licensed from UC’s Office of Entrepreneurial Affairs and Technology Commercialization. Its CEO is Rick Hawkins, a 30-year biotech industry veteran. Jon Saxe is its chairman. “It has taken many years to get here and I am happy that our efforts have led to this translational effort to make a therapy available to those afflicted with CTD,” says Clark. “We look forward with commitment and hope to the day when those patients will benefit from our work.” The collaboration gained momentum when Lumos Pharma submitted a proposal based on Clark’s technology to the National Institutes of Health and was selected as a drug development project partner by the National Center for Advancing Translational Sciences’ Therapeutics for Rare and Neglected Diseases (TRND) program. Under TRND’s collaborative operational model, project partners form joint project teams with TRND and receive in-kind support from TRND drug development scientists, laboratory and contract resources. Lumos Pharma plans to initiate a TRND-supported preclinical development plan, with TRND support continuing through the filing of an Investigational New Drug (IND) application with the FDA prior to beginning a clinical trial. Such a trial would be about three years away, Clark says. In addition to Clark, study team members are Yuko Kurosawa, PhD; Ton de Grauw, MD, PhD; Diana Lindquist, PhD; Victor Blanco, PhD; Gail Pyne-Geithman, DPhil; Takiko Daikoku, PhD; James Chambers, PhD; and Stephen Benoit, PhD. ### The research by Clark’s team was supported by funding from the National Institutes of Health. The study authors report no conflicts of interest. Contact: Keith Herrell |
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