Research Roundup: Some of the Top Research Stories of the Week
There is almost always exciting research going on every day. Here are just a few that caught BioSpace’s attention this week.
- The technical journal, Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association, published the “NIA-AA Research Framework: Towards a Biological Definition of Alzheimer’s Disease.” The authors, led by Clifford Jack of Mayo Clinic, proposed changing the definition of Alzheimer’s disease in living people for use in research. It would shift the current definition, which is based on cognitive changes and behavioral symptoms with biomarker confirmation, to a solely biological construct.
- Also in Alzheimer’s research, Nature Medicine published an article by Wang Chengzhong et al. with the Gladstone Institutes, which revealed how ApoE4 increased risk for Alzheimer’s disease in human cells. They were also able to reverse the damage caused by ApoE4 by using a small molecule to change the molecule into a harmless ApoE3-like version.
- Three studies published in the journal Cell, focus on how kidney cancer starts and progresses. One of the papers, by researchers at Sanger Institute in Cambridge, UK, describe how the genetic abnormalities that lead to cancer can be seen decades before the primary tumor is diagnosed. The other papers, one by lead author Samra Turajlic, at the Francis Crick Institute in London, describes three distinct evolutionary pathways that leads to kidney cancer. This could lead to more accurate prognoses and personalized treatments.“Knowing the next step in cancer’s evolutionary trajectory could tailor the treatment choice for individual patients,” Turajlic told Forbes. “Patients with the least aggressive tumors could be spared surgery and monitored instead and those with gradually evolving tumors could have the primary tumor surgically removed even after it has spread.”
- Researchers at the University of Copenhagen identified a variation of gene FGF21 that that appears to be linked to a predisposition to less body fat. A year ago the same gene seemed to show why some people have a “sweet tooth,” because they seem to eat more sugar than other people. But the gene variant also appears linked with increased blood pressure and more fat around the waist, the so-called “apple shape.” It was published in the journal Cell Reports, and was conducted in collaboration with researchers at the University of Exeter Medical School. In a statement, Niels Grarup, associate professor at the University of Copenhagen and a member of the Novo Nordisk Foundation Center for Basic Metabolic Research, said, “This is just a small piece of the puzzle describing the connection between diet and sugar intake and the risk of obesity and diabetes.”
- There has been plenty of news over the last couple years about how sitting is bad for you. Now a new study by Prabha Siddarth et al. and others with the University of California Los Angeles (UCLA) published in PLOS One, found that sitting and a sedentary lifestyle is associated with reduced medial temporal lobe thickness in middle-aged and older adults. Participants answered questions about their physical activity and how much time they spent sitting, and were tested for Alzheimer gene variants ApoE, and given MRI scans that measured the thickness of the medial temporal lobe. The authors wrote in the paper, “It is possible that sedentary behavior is a more significant predictor of brain structure, specifically [medial temporal lobe] thickness, and that physical activity, even at higher levels, is not sufficient to offset the harmful effects of sitting for extended periods of time.” There didn’t appear to be a link between ApoE and thickness in the area, though.
- And finally, researchers at Sydney, Australia’s Garvan Institute of Medical Research published a study in Science that provides a deeper understanding of the human body’s immune system. The study outlines how certain “bad” antibodies in the immune system that are typically silenced because of the damage they cause within the body, also provide crucial protection against microbes. The research was conducted on mice. The antibodies in question are typically associated with autoimmune disease, but the research suggests that these antibodies, which are often inactive for long periods of time, may go through a fast “redemption” process and are activated when the body faces infections or attackers that the rest of the immune system can’t handle. Co-lead researcher, Chris Goodnow, told Science Daily, “We once thought that harmful antibodies were discarded by the body—like a few bad apples in the barrel—and no one had any idea that you could start with a ‘bad’ antibody and make it good. From these new findings, we now know that every antibody is precious when it comes to fighting invading microbes—and this new understanding means that ‘bad’ antibodies are a valuable resource for the development of vaccines for HIV, and for other diseases that go undercover in the body.”