There are plenty of great scientific research stories out this week. Here’s a look at just a few of them.
Owning a Dog? It’s in Your Genes
Researchers at Uppsala University in Sweden and the University of Liverpool, using data on 35,035 twin pairs from the Swedish Twin Registry found that the choice of owning a dog is significantly influenced by a person’s unique genetic make-up. The research was published in the journal Scientific Reports.
“We were surprised to see that a person’s genetic make-up appears to be a significant influence in whether they own a dog,” stated Tove Fall, lead author and Professor in Molecular Epidemiology at the Department of Medical Sciences and the Science for Life Laboratory at Uppsala. “As such, these findings have major implications in several different fields related to understanding dog-human interaction throughout history and in modern times. Although dogs and other pets are common household members across the globe, little is known about how they impact our daily life and health. Perhaps some people have a higher innate propensity to care for a pet than others.”
The research found that rates of dog ownership were much higher in identical twins than in non-identical twins. Although the study doesn’t identify which genes are involved, it suggests that genetics and environment play about equal roles in determining dog ownership.
Pancreatic Beta Cells May Change Function in Diabetes
Pancreatic beta cells are the cells that produce insulin. A new study out of the University of Exeter has found that the RNA messaging system in diabetes cells that tells cells how to behave is different than in non-diabetes beta cells. The changes cause some of the beta cells to no longer produce insulin and instead produce somatostatin, which potentially blocks the secretion of other hormones, including insulin. The research was published in the journal Human Molecular Genetics.
“These insights are really exciting,” stated Lorna Harries, who led the research. “Only recently, Exeter researchers discovered that people with type 1 diabetes still retain some insulin-producing cells, but the environment produced by diabetes can be toxic for these cells that remain. Our work could lead to new changes to protect these cells, which could help people maintain some ability to make their own insulin. The method we used of creating an all-human cell system for the first time is significant—I don’t think we’d have seen these changes in mouse cells.”
The research team utilized entirely animal-free models, using a completely human cell system. Beta cell loss happens in both types 1 and 2 diabetes. Previous research has suggested the cell loss was related to the microenvironment around the cells. But this research found that a proportion of the cells are no longer beta cells producing insulin. A much higher proportion of delta cells were observed. In animal models, there were similar findings, but the changes are different. In mice, most of the changes are beta cells to alpha cells, not delta cells. Alpha cells produce the hormone glucagon.
Harries stated, “The really exciting finding is that in the laboratory at least, we have been able to reverse the changes—turn the delta cells back to beta cells—if we restore the environment to normal, or if we treat the cells with chemicals that restore the regulator genes and the patterns of RNA messages made to normal. That’s very promising when we consider the potential for new therapeutics.”
Gut Bacteria and Anxiety
The entire field of studying the microbiome is the premise that the trillions of microorganisms that live in your body play a larger role in your health than just gut health. These microorganisms appear to have a broad range of effects via cellular signaling and microenvironments than previously believed. Researchers from the Shanghai Jiao Tong University School of Medicine recently published a study in the journal General Psychiatrylinking regulation of gut bacteria to anxiety.
The researchers reviewed 21 studies that evaluated 1,503 people collectively. Of the 21 studies, 14 had utilized probiotics as interventions for regulating intestinal microbiota (IRIFs). Seven picked non-probiotics, such as adjusting daily diets. The researchers found that the probiotic supplements in seven studies involved only one kind of probiotic, while two studies used a product containing two types of probiotics. The supplements used in the other five had at least three kinds of probiotics.
Eleven of the 21 studies indicated a positive effect on anxiety symptoms by regulating intestinal bacteria. Of the 14 that used probiotics, 36% were effective in reducing anxiety symptoms, and six of the seven remaining studies using non-probiotics had an 86% rate of effectiveness. The researchers wrote, “We find that more than half of the studies included showed it was positive to treat anxiety symptoms by regulation of intestinal microbiota.”
New Mechanism of Cell Death in Alzheimer’s Identified
Researchers with the Van Andel Research Institute (VARI) have identified a new mechanism that speeds aging in the brain and precedes the most damaging biological aspects of Alzheimer’s disease. They published their research in the journal Nature Communications.
The findings focus on “enhancers,” which can turn the activity of genes up or down based on various influences such as aging and environmental factors. They evaluated 1.2 million CpG and CpH sites in enhancers in prefrontal cortex neurons in people that had no AD, mild, moderate and severe AD. The team identified 1,224 differentially methylated enhancer regions, most at CpH sites in AD neurons. CpH methylation losses happen during normal aging but are accelerated in Alzheimer’s. They also found that the enhancers over-activate a set of genes involved in Alzheimer’s in brain cells, which stimulates the formation of plaques and tangles, and reactivates the cell cycle in fully formed cells.
“In adults, brain cells are done dividing,” stated Viviane Labrie, senior author of the study and assistant professor at VARI. “The enhancer changes we found also encourage the development of plaques, which act as gasoline for the spread of toxic tangles, propagating them through the brain like wildfire. Taken together, enhancer abnormalities that promote plaques, tangles and cell cycle reactivation appear to be paving the way for brain cell death in Alzheimer’s disease.”
Placental Stem Cells that Can Regenerate Heart After a Heart Attack
Researchers at the Icahn School of Medicine at Mount Sinai have shown that stem cells derived from the placenta, called Cdx2 cells, can regenerate healthy heart cells after heart attacks. At least in animals. They published their research in the Proceedings of the National Academy of Sciences (PNAS).
“Cdx2 cells have historically been thought to only generate the placenta in early embryonic development, but never before were shown to have the ability to regenerate other organs, which is why this is so exciting,” stated Hina Chaudhry, principal investigator and Director of Cardiovascular Regenerative Medicine at Icahn. “These findings may also pave the way to regenerative therapy of other organs besides the heart. They almost seem like a super-charged population of stem cells, in that they can target the site of an injury and travel directly to the injury through the circulatory system and are able to avoid rejection by the host immune system.”
Working with mice, the research team induced heart attacks in three groups of male mice. One group was given Cdx2 stem cells derived from end-gestation mouse placentas. One group received placenta cells that didn’t express Cdx2. The third group was given a saline control. Using MRI to analyze the mice immediately after the heart attacks and three months after receiving the stem cell transplants, they found that all the mice in the Cdxw stem cell treatments showed significant improvement and regeneration of healthy tissue in the heart. At three months, the stem cells had migrated to the heart injury and formed new blood vessels and new cardiomyocytes, which are beating heart muscle cells. The non-Cdx2 and placebo groups went into heart failure with no evidence of heart muscle regeneration.
Monkey Virus May be Part of HIV Vaccine
Researchers at The Scripps Research Institute in La Jolla, Calif. are working on a vaccine for HIV, and believe that a protein from Simian Immunodeficiency Virus (SIV) may play a key role. SIV causes an AIDS-like disease in monkeys and apes and it is believed that the virus jumped to humans and evolved into HIV about 100 years ago in Africa. SIV’s outer-envelope protein, Env, has a key structure with HIV’s Env. They published their research in the journal Cell Reports.
“We’ve shown here that one can use shapes from chimpanzee-infecting SIV to stimulate the production of antibodies against the human-infecting HIV,” stated co-senior author Dennis Burton, the James and Jessie Minor Chair in Immunology in the Department of Immunology and Microbiology at Scripps. “It’s a simple but inspired strategy, reminiscent of the use of cowpox virus to immunize against smallpox virus over 200 years ago, and should help us in making an HIV vaccine.”
Typical vaccines utilize a weakened or engineered version of a virus to stimulate the immune system to produce antibodies against it. But in HIV, this approach doesn’t work because the virus quickly mutates its outer structures during infection. Burton and his team are working on designing HIV vaccines that stimulate the antibody response on the most vulnerable virus parts, but they are typically hidden by the virus. The known antibodies that do this, which are rare, also have unusual shapes and are difficult for the immune system to create. Burton’s team hopes to move past those obstacles by using a primary injection followed by a series of booster shots, each with distinct immunogens, that will slowly force the production of those antibodies.