A recent study in mice was able to halt memory decay in a model of Alzheimer’s disease. Another study found that even mild infection increased the risk of new-onset type 2 diabetes, although the risk increased with the severity of COVID-19.
Although researchers haven’t solved the problem of Alzheimer’s disease yet, an enormous amount of research into the disease is being done, deepening our understanding of its pathology. And a recent study in mice was able to halt memory decay in a model of the disease. For that and more research news, read on.
Halting Memory Degradation in Experimental Alzheimer’s Model
Researchers at Louisiana State University Health Sciences Center and Sweden’s Karolinska Institute applied specialized pro-resolving lipid mediators intranasally in a rodent model of Alzheimer’s disease and halted memory decay. One hallmark of neurodegenerative disorders is neuroinflammation. The specialized pro-resolving lipid mediators are bioactive compounds made up of fatty acids like omega-3 or their derivatives known to minimize inflammation. One of those compounds is Neuroprotectin D1 (NPD1), discovered by Dr. Nicolas Bazan, Boyd professor and director of the LSU Health New Orleans Neuroscience Center of Excellence and his colleagues. Earlier studies found that NPD1 is protective in experimental stroke, retinal damage, and at low levels in the memory area in brain samples from Alzheimer’s patient donors. They published their research in Communications Biology.
“AD lacks prevention or cure and exerts a horrendous toll on patients and their families due to crippling progression and devastating adverse events,” said Dr. Bazan. “Millions of Americans currently suffer from AD, and the number is expected to escalate rapidly in the coming years.”
In the mouse model, the intranasal application of NPD1, resolving (Rv) E1, RvD1, RvD2, Maresin 1 (MaR1), a selection of pro-resolving lipid mediators, resulted in halting memory deficits while restoring gamma oscillation deficits. Together, they created a dramatic decrease in microglial activation. Microglial overactivation and increased pro-inflammatory signaling are associated with chronic inflammation and neuronal damage in Alzheimer’s disease.
The authors wrote, “In conclusion, we report that intranasal delivery is a non-invasive administration route for LMs that impact the central nervous system. Consequently, we uncover beneficial effects of pro-resolving LMs by improving cognitive functions, rescuing disrupted gamma activity and reducing microglial activation in the AppNL-G-F model…. This study supports the potential therapeutic intranasal delivery of LMs in AD, other neurodegenerative diseases, and various forms of brain injury.”
White-Tailed Deer Can Transmit COVID-19 5 Days After Infection
It’s already been established that white-tailed deer are a potential reservoir for COVID-19. A new study from Cornell University found that the deer can shed and transmit the virus for up to five days once they are infected. They view this as a “relatively short window of time.” The virus develops and replicates in the animal’s respiratory tract, lymphoid tissues — including tonsils and lymph nodes — and the CNS. The upper respiratory tract and nose replication are similar to what is seen in humans and other animals susceptible to COVID-19. They hope the data will assist in surveillance of infections in the deer to provide hunters with helpful information during hunting season. There is currently no data showing that humans have caught COVID-19 from deer, although researchers worry it might be possible.
Sugar Consumption and Inflammation
High levels of long-term sugar and carbohydrate consumption are associated with an increased risk of autoimmune diseases. This includes diseases like inflammatory bowel diseases like Crohn’s and ulcerative colitis, type 1 diabetes and chronic inflammation of the thyroid gland. Although there are many molecular mechanisms behind autoimmune diseases, researchers at the Julius Maximilians University of Wurzburg (JMU) found that excessive consumption of glucose (sugar) directly promotes pathogenic aspects of specific immune cells. At the same time, a low-calorie diet can benefit the immune system. They specifically looked at a glucose transporter, GLUT3, with metabolic functions in T immune cells. Specifically, T helper type 17 cells (Th17) express large amounts of GLUT3 protein on their cell surface. Once they take up glucose, it is converted to citric acid in the mitochondria then metabolized into acetyl-coenzyme A in the cytoplasm. Acetyl-CoA is involved in the biosynthesis of lipids, but also functions in inflammatory Th17 cells.
The Problem with Smartwatch Heart Data
Increasingly, consumers are using smartwatches such as the Apple Watch or a Fitbit or other wearable devices to measure heart rate and other metrics. They are even being used in clinical trials. There is a problem, however. Researchers at the University of Alberta in Edmonton, Canada conducted a systematic review of 10 previously published studies of these devices, specifically looking at how skin tone affects the devices’ accuracy. They started with 622 scientific papers and identified 10 that reported race or skin tone data. Of them, four indicated that heart rate measurements were significantly less accurate in darker-skinned individuals than lighter-skinned people or against measurements from validated devices, such as electrocardiograms and chest strap monitors. One study suggested no difference in heart rate accuracy, but wearable devices recorded significantly fewer data points for darker-skinned individuals. Typically, these devices detect heart rate and rhythm by shooting a light beam at the wrist and detecting how much light is absorbed.
COVID-19 Increases Risk of Type 2 Diabetes
A large cohort study was published in The Lancet Diabetes & Endocrinology and looked at national databases from the U.S. Department of Veterans Affairs to evaluate 181,280 participants who tested positive for COVID-19 between March 1, 2020, and September 30, 2021, and survived the first 30 days of COVID-19. They then used a contemporary control of 4,118,441 people and a historical control of 4,286,911 that had no history of COVID-19 infection. Participants in all three cohorts were “free of diabetes before cohort entry and were followed up for a median of 352 days.”
The study found that even mild infection increased the risk of new-onset type 2 diabetes, although the risk increased with the severity of COVID-19 symptoms. The study doesn’t demonstrate cause and effect but suggests a strong association between COVID-19 infection and type 2 diabetes. Individuals diagnosed with COVID-19 were 46% more likely to develop type 2 diabetes for the first time or to be prescribed drugs to control their blood sugar.
“For the broader public, if you’ve had COVID-19, you need to pay attention to your blood sugar,” Ziyad Al-Aly, MD, chief of research and development at VA St. Louis Health Care System who led the review, said.
