Welcome to this week’s Research Roundup. These Friday posts aim to inform our readers about the many stories that relate to animal research each week. Do you have an animal research story we should include in next week’s Research Roundup? You can send it to us via our Facebook page or through the contact form on the website.
- Alzheimer’s “cocktail” developed with mouse studies. Researchers at the Yale School of Medicine have developed a drinkable medicine that, in mice, interferes with a critical first step in the development of Alzheimer’s disease. The “cocktail” also restored some memory deficits in the animals. In Alzheimer’s amyloid beta peptides bind to prions in the brain, leading to the accumulation of plaques, damage to synapses, and a destructive immune response. After screening tens of thousands of compounds, the scientists discovered that an antibiotic was a promising candidate to interfere with this devastating interaction, but only after it decomposed to form a polymer. The researchers then dissolved the polymer and fed it to Alzheimer’s-like mice, finding that brain synapses were repaired and lost memory was recovered. The next crucial contribution of animal research will be to verify that the medicine isn’t toxic, so it can be prepared for clinical trials. Published in Cell Reports.
- Treatment for urinary incontinence receives a “green light”. Urinary incontinence affects approximately 30% of women and 1.5-5% of men between the ages of 30-60. It is, unsurprisingly, associated with a diminished quality of life. New research on a fully implantable device, and where proof of principle was tested in rats, may provide a solution. The device has three main parts: two green LED lights, a metal ring that wraps around the bladder, and a thin control center. The metal rings measures the size of the bladder and when excessive urination occurred in a hour, the green lights turned on. The green lights, activated a light sensitive protein (thanks to gene therapy) which blocked signals from being sent from the bladder to the brain–resulting in an overall decrease of urination frequency. Because bladder function is quite similar in rats and humans, it is hoped that this device (with a few modifications) may one day be used in humans. Published in Nature.
- Hormone released during exercise protects against Alzheimer’s. Scientists at the Federal University of Rio de Janeiro have discovered that the hormone; irisin, is key for physical exercise to protect against Alzheimer’s. They first identified that human Alzheimer patients had lower levels of irisin than healthy controls. Next, they blocked irisin in mice genetically engineered to have symptoms of Alzheimer’s. When these mice, with blocked irisin, engaged in physical exercise, they showed no protection against developing Alzheimer’s. Because it is well known that exercise protects against Alzheimer’s and irisin is released during exercise, it is likely that irisin is a key chemical for protecting against Alzheimer’s, not just exercise alone. Published in Nature Medicine.
- The potential role of the gut microbiome and starchy foods in lupus. Lupus is an autoimmune disease where the body’s own immune system attacks the body. It is estimated that 5 million people around the world have lupus. Suspecting a role of the gut microbiome, and using a mouse model of lupus, researchers at Yale University gave antibiotics to mice as a means of reducing levels of gut bacteria. They found that mice provided with antibiotics (as compared to those that did not) had less severe autoimmune responses and were twice as likely to survive. Unhealthy mice, also had high levels of lactobacillus which spread to the intestines, livers and spleens as compared to healthy mice. Finally, because starchy food can halt the growth of certain gut bacteria, the team fed a starch diet to mice for 7 months, and found that there was less growth of lactobacillus, less transfer of these bacteria to other parts of the body, and a general improvement in symptomatology. Published in Cell Host & Microbiome.
- Researchers correct genetic mutation that causes IPEX, a life-threatening autoimmune syndrome. UCLA researchers have created a method for modifying blood stem cells to reverse the genetic mutation that causes immune dysregulation, polyendocrinopathy, enteropathy, X-linked (IPEX). The gene therapy, which was tested in mice, is similar to the technique used by these researchers to cure patients with severe combined immune deficiency (SCID); another immune disease. IPEX is caused by a mutation that prevents a gene called FoxP3 from making a protein needed for blood stem cells to produce immune cells called regulatory T cells. Regulatory T cells keep the body’s immune system in check; without them, the immune system attacks the body’s own tissues and organs, which is known as autoimmunity. The approach adds a normal copy of the FoxP3 gene to blood stem cells, which can produce all types of blood cells. In the study, the approach corrected the genetic mutation in mice with a version of IPEX that’s similar to the human version of the disease, and it restored proper immune regulation. Published in Cell Stem Cell.