Research Roundup: Preventing Type 1 Diabetes and More

Every week there are numerous scientific studies published. Here’s a look at some of the more interesting ones.

Every week there are numerous scientific studies published. Here’s a look at some of the more interesting ones.

Protein Protects Pancreatic Cells in Animal Model of Type 1 Diabetes

Investigators with the University of Southern California found that a small protein, MOTS-c, kept the immune system from killing insulin-producing pancreatic cells, basically preventing type 1 diabetes in laboratory mice. MOTS-c first made the news as an “exercise mimetic” because of its role in regulating the immune system. Type 1 diabetes is an autoimmune disease where the immune system attacks the insulin-producing islet cells in the pancreas. It makes up 5% to 10% of diabetes cases. The research suggested that MOTS-c supports regulatory T-cells, the immune cells that recognize which cells belong to the body, and decrease activation of killer T-cells, that incorrectly attack healthy islet cells. The research was published in Cell Reports.

“We are able to prevent the onset of type 1 diabetes in mouse models,” said Changhan David Lee, co-corresponding author of the study and assistant professor of Gerontology at USC.

MOTS-c is one of a number of recently discovered hormones encoded in the DNA of mitochondria, the energy factories of cells. The majority of hormones are otherwise encoded in DNA in the nucleus. Lee and his colleague Pinchas Cohen, dean of the USC Leonard Davis School, first described MOTS-c in 2015. It was then found to be involved in restoring insulin sensitivity and counteracting diet-induced and age-dependent insulin resistance, which is typically linked to exercise.

“The mitochondrial genome encodes for previously unknown genes that yield small proteins with multiple physiological roles, including aging, exercise, metabolism, and immunity,” Lee said. “Further studies on the molecular mechanism of these mitochondrial-encoded peptides are ongoing and may provide novel therapeutic targets for autoimmune conditions, which increases as we age.”

Is Blood Clotting Root Cause of Long COVID Syndrome?

A study by researchers from RCSI University of Medicine and Health Sciences found that patients with Long COVID syndrome, sometimes called “long-haulers,” have higher measurements of blood clotting. They believe this might be behind the persistent symptoms, which include decreased physical fitness and fatigue. The study followed 50 patients with symptoms of Long COVID syndrome and found that clotting markers were significantly higher in their blood compared with healthy controls. The markers were higher in patients who had been hospitalized with their initial COVID-19 infection but were found even in people who could manage their disease at home.

T-Cells and Antibodies in Response to mRNA COVID-19 Vaccines

Scientists with the University of Pennsylvania School of Medicine found that the mRNA vaccines stimulated a fast and strong response by T-cells. Much of the news about immune responses by the vaccines have been focused on antibody response, but the T-cell response is also important and may reflect more durable protection. In the study, which was published in Immunity, the researchers analyzed T-cell responses in 47 healthy people who received two doses of the Moderna and Pfizer-BioNTech mRNA COVID-19 vaccines. The data showed a robust T-cell response after the first dose with no significant increase after the second dose. This has potential implications for the booster shots. They believe they will need larger follow-up studies to better understand the implications of their findings.

Gene-Editing for Alzheimer’s Disease?

Investigators at Hong Kong University of Science and Technology developed a brain-wide genome-editing technology that decreased Alzheimer’s disease pathologies in genetically modified Alzheimer’s mouse models. The genome-editing system crosses the blood-brain barrier and delivers an optimized genome-editing tool to the whole brain. The delivery system is a new approach which is via a single non-invasive intravenous administration. The technique disrupted FAD (Familial Alzheimer’s Disease)-inflicted mutations in the mice, which decreased the level of amyloid. Amyloid is a protein that accumulates abnormally in the brains of Alzheimer’s patients. The treatment decreased amyloid and kept it low for six months after treatment, which in mice is about a third of their normal lifespan. No side effects have yet to be observed.

Alzheimer’s Might Start Inside Nerve Cells

A study out of Lund University in Sweden suggests that amyloid-beta, the protein that abnormally accumulates in the brains of Alzheimer’s disease, may actually start accumulating inside nerve cells. Then misfolded protein then spreads to cells by way of nerve fibers. This appears to occur much earlier than the formation of amyloid-beta plaques in the brain, which is associated with the progression of Alzheimer’s disease. The research builds on amyloid-beta’s prion-like properties. Prions are misfolded proteins that are behind “mad-cow” disease and Creutzfeldt-Jakob disease. The research suggests that amyloid-beta is extremely important to Alzheimer’s pathology, but that research should focus on disrupting it even earlier when it is inside the nerve cells. Amyloid-beta is observed in the brains of healthy people, but how and why it misfolds and abnormally accumulates isn’t clear.

Babies and Toddlers Spread COVID-19 in Homes More than Teens

Babies and toddlers aren’t called “germ factories” for nothing. A new study by a Canadian public health agency reports that babies and toddlers aren’t as likely to bring COVID-19 into their homes than teenagers—likely because they don’t get out as much. However, once they are infected, babies and toddlers are more likely to spread the disease to the rest of the household. The study was published in JAMA Pediatrics.

“This study showed that even the youngest of children readily transmit the virus,” Zoe Hyde, an epidemiologist at the University of Western Australia, who was not involved in the research, told The New York Times. “The key takeaway for me is that it clearly shows that there’s transmission from children occurring in the households. This means we urgently need to think about how we’re going to protect schools when they reopen shortly.”

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