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Archive - Sep 14, 2017

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Study Highlights Possible Key Role of TOMM40 Gene Variant in Alzheimer’s Disease

The notorious genetic marker of Alzheimer's disease and other forms of dementia, ApoE4, may not be a lone wolf. Researchers from the University of Southern California (USC) and the University of Manchester have found that another gene, TOMM40 (image depicts TOMM40 protein), complicates the picture. Although ApoE4 plays a greater role in some types of aging-related memory ability, TOMM40 may pose an even greater risk for other types. TOMM40 and APOE genes are neighbors, adjacent to each other on chromosome 19, and they are sometimes used as proxies for one another in genetic studies. At times, scientific research has focused chiefly on one APOE variant, ApoE4, as the No. 1 suspect behind Alzheimer's and dementia-related memory decline. The literature also considers the more common variant of APOE, ApoE3, neutral in risk for Alzheimer's disease. USC researchers believe their new findings raise a significant research question: Has TOMM40 been misunderstood as a sidekick to ApoE4 when it is really a mastermind, particularly when ApoE3 is present? "Typically, ApoE4 has been considered the strongest known genetic risk factor for cognitive decline, memory decline, Alzheimer's disease, or dementia-related onset," said Dr. T. Em Arpawong, the study's lead author and a post-doctoral fellow in the USC Dornsife College of Letters, Arts and Sciences Department of Psychology. "Although prior studies have found some variants of this other gene TOMM40 may heighten the risk for Alzheimer's disease, our study found that a TOMM40 variant was actually more influential than ApoE4 on the decline in immediate memory - the ability to hold onto new information." Studies have shown that the influence of genes associated with memory and cognitive decline intensifies with age.

Caloric Restriction Slows Epigenetic Drift and Slower Epigenetic Drift May Be Mechanism Underlying Lifespan Extension

Almost a century ago, scientists discovered that cutting calorie intake could dramatically extend lifespan in certain animal species. Despite numerous studies since, however, researchers have been unable to explain precisely why. Now, investigators at the Lewis Katz School of Medicine at Temple University (LKSOM) have broken past that barrier. In new work published online on September 14, 2017 in Nature Communications, they are the first to show that the speed at which the epigenome changes with age is associated with lifespan across species and that calorie restriction slows this process of change, potentially explaining its effects on longevity. The article is titled “Caloric Restriction Delays Age-Related Methylation Drift.” "Our study shows that epigenetic drift, which is characterized by gains and losses in DNA methylation in the genome over time, occurs more rapidly in mice than in monkeys, and more rapidly in monkeys than in humans," explains Jean-Pierre Issa, MD, Director of the Fels Institute for Cancer Research at LKSOM, and senior investigator on the new study. The findings help to explain why mice live only about two to three years on average, rhesus monkeys about 25 years, and humans 70 or 80 years. Chemical modifications such as DNA methylation control mammalian genes, serving as bookmarks for when a gene should be used - a phenomenon known as epigenetics. "Methylation patterns drift steadily throughout life, with methylation increasing in some areas of the genome, and decreasing in others," says Dr. Issa. Previous studies had shown that these changes occur with age, but whether they were also related to lifespan was unknown.Dr. Issa's team made its discovery after first examining methylation patterns on DNA in blood collected from individuals of different ages for each of three species - mouse, monkey, and human.

Invitation to ASEMV 2017 Annual Meeting (Exosomes & Microvesicles) in Asilomar, California (October 8-12)

The American Society for Exosomes and Microvesicles (ASEMV) is inviting interested scientists to the ASEMV 2017 meeting, to be held October 8-12, 2017 at the Asilomar Conference Center in California. This center is located on the Monterrey peninsula, just south of San Francisco (www.visitasilomar.com). The meeting will cover the full breadth of the exosome field, from basic cell biology to clinical applications, and follow the ASEMV tradition of inclusion and diversity as participants learn about the latest advances in the field. ASEMV 2017 is a forum for learning the latest discoveries in the field of exosomes, microvesicles, and extracellular RNAs. Over the course of four days at the Asilomar Conference Center, ASEMV 2017 will offer presentations from leading scientists and young researchers. Topics will span the breadth of the extracellular vesicle/RNA field, including the basic sciences, disease research, translation efforts, and clinical applications. Talks will be presented in multiple sessions, beginning at 7 pm on Sunday, October 8, 2017, and concluding at 4 pm on Thursday, October 12, 2017. Poster sessions will run throughout the meeting, with ample time to get to know your colleagues in the field and explore the many opportunities in this rapidly expanding field. Please see the links below.

Researchers Find a Possible New Treatment for Aggressive Triple-Receptor-Negative Breast Cancer; New Inhibitor of Cancer Stem-Like Cells Brings New Hope

Scientists from the cluster of excellence BIOSS Centre for Biological Signaling Studies at the University of Freiburg and the Freiburg University Medical Center in Germany have shown that inhibiting the epigenetic regulator KDM4 might offer a potential novel treatment option for breast cancer patients. They used a newly established cell model that enables scientists to isolate cancer stem cells directly from patient tumor. Using this special culture system, they were able to test potential new cancer drugs. One of these, a novel inhibitor of the epigenetic regulator KDM4, co-developed in the lab of Professor Roland Schüle, showed promising results. The researchers published their work online on September 7, 2017 in Cancer Research. The article is titled “KDM4 Inhibition Targets Breast Cancer Stem-Like Cells.” Although the prognosis for breast cancer has been steadily improving in the last decades, patients with triple-receptor-negative breast cancer form a subgroup who receive a considerably worse prognosis in most cases. Roughly 15 percent of all breast cancer patients have triple-receptor-negative breast cancer, which lacks markers for a targeted therapy. In the last few years, a bulk of data pointing to a small population of cells in tumors that maintain tumor growth, are particularly resistant to chemotherapy, are responsible for relapses, and develop metastases. These cells, named cancer stem-like cells, share many characteristics with the body’s normal stem cells. Due to their cancer-driving behavior, researchers have been focusing more and more on targeting these cells. However, there are currently only a few models available to study the biology of cancer stem cells.