Every week there are numerous scientific studies published. Here’s a look at some of the more interesting ones.
A study in mice by The National Institutes for Quantum Science and Technology in Japan found that a low protein diet can accelerate brain degeneration in an Alzheimer’s mouse model. But more significantly, they found that a supplement with seven specific amino acids called Amino LP7, appeared to slow brain degeneration and dementia development in the animals. They published their research in Science Advances.
“In older individuals, low protein diets are linked to poor maintenance of brain function,” said Makoto Higuchi, one of the lead scientists of the study. “Amino acids are the building blocks of proteins. So, we wanted to understand whether supplementation with essential amino acids can protect the brains of older people from dementia, and if yes, what mechanisms would contribute to this protective effect.”
Mice on a low protein diet had accelerated brain deceleration as well as poor neuronal connectivity. But the effects were reversed after receiving Amino LP7, which suggested those seven specific amino acids might inhibit brain damage. They then studied how Amino LP7 affects different types of brain degeneration in their model. For example, untreated mice had high levels of progressive brain degeneration, but Amino LP7 suppressed neuronal death, which decreased brain degeneration, even though the mice brains still had Tau aggregates. Tau plaques are characteristic of Alzheimer’s. They also analyzed the gene-level changes caused by Amino LP7, which suggested the supplement decreased brain inflammation and prevented kynurenine an inflammation inducer, from entering the brain.
“These results suggest that essential amino acids can help maintain balance in the brain and prevent brain deterioration,” said Hideaki Sato and Yuhei Takado, both contributors to the research. “Our study is the first to report that specific amino acids can hinder the development of dementia. Although our study was performed in mice, it brings hope that amino acid intake could also modify the development of dementias in humans, including Alzheimer’s disease.”
Lab-Grown Mini Brains, ALS and Frontotemporal Dementia
Researchers at the University of Cambridge developed “mini brains” that can be used to study amyotrophic lateral sclerosis, which often overlaps with frontotemporal dementia (FTD). And for the first time, they’ve managed to grow these organoids for almost a year. The team used stem cells from patients with ALS/FTD to grow brain organoids. They are similar to parts of the human cerebral cortex in terms of embryonic and fetal developmental milestones, 3D architecture, cell-type diversity and cell-cell interactions. This has been done before, but what was new was they were able to grow them for so long; and they had the most common genetic mutation in ALS/FTD. The published research has them growing for 240 days, but an unpublished manuscript shows they have grown for 340 days.
Malaria Drug Might Help Fight COVID-19
A study published in the journal ACS Infectious Diseases evaluated the potential of atavaquone against the Wuhan wildtype strain of SARS-CoV-2 and other variants of concern. The study tested the drug in cell cultures infected with several different strains of COVID-19. The data showed a dose-dependent block in the infectivity.
Anecdotal evidence from 17 patients in Quebec and Ontario, Canada, had suggested that malarone/atovaquone might have a preventive effect. So the researchers decided to test the drugs in cell cultures to evaluate the antiviral potential. They found that it “potently inhibits the replication of SARS-CoV-2 and other variants of concern including the alpha, beta, and delta variants. Importantly, atovaquone retained its full antiviral activity in a primary human airway epithelium cell culture model.”
Two clinical trials were initiated in the U.S. in 2020 to evaluate atovaquone alone or in combination with azithromycin, but the results have still not been reported. This new study suggests that the drug may be a strong antiviral against COVID-19.
Blocking Bach1 Protein Slows Deterioration of Brain Cells in Parkinson’s
Investigators at the Medical University of South Carolina (MUSC) identified a novel role for the regulatory protein Bach1 in Parkinson’s disease. They found that Bach1 levels were higher in postmortem Parkinson’s disease-affected brains, while cells without Bach1 seemed to be protected from the damage that accumulates in Parkinson’s. Working with vTv Therapeutics, they identified a drug, HPPE, which is a potent inhibitor of Bach1. This seems to protect cells from inflammation and the buildup of toxic oxidative stress when given before or after the onset of Parkinson’s symptoms. They believe this is the first evidence that Bach1 is dysregulated in Parkinson’s disease. Many of the inflammation and toxic oxidative stress pathways are controlled by two proteins, Nrf2 and Bach1. Nrf2 turns on the expression of more than 250 genes involved in protecting cells from these stressors, while Bach1 prevents the genes from being activated. In mouse studies, HPPE appeared to alleviate symptoms of Parkinson’s and to protect neurons from destructive pathways by switching on antioxidant genes and switching off pro-inflammatory genes.
Type 1 Diabetes Might Be More Than a Single Disease
New research from the international The Environmental Determinants of Diabetes in the Young (TEDDY) study added support to the theory that type 1 disease is not just one disease. The study found that the cause of autoimmune diabetes seems to vary in genetically high-risk children. The study, which was published in Diabetologica by Jeffrey Krischner, director of the Health Informatics Institute at the University of Southern Florida Health Morsani College of Medicine, compared the traits of type 1 diabetes diagnosed in children before and after the age of 6.
Type 1 diabetes is an autoimmune disease where the immune system attacks the person’s pancreatic beta cells, which are the cells that produce insulin. Four specific autoantibodies directed against beta cells are the most reliable biological indicators of early type 1 diabetes before symptoms are observed: glutamic acid decarboxylase autoantibody (GADA), insulin autoantibody (IA), insulinoma-associated-protein-2 autoantibody (IA2-2A), and zinc transporter 8 autoantibody (ZnT8A). But not all children who test positive for one or more of those antibodies end up diagnosed with type 1 diabetes. Their research found out more about the order, timing and type of autoantibodies, which can help predict which children are most likely to be diagnosed with type 1 diabetes as they get older.
“Our results underscore the importance of taking into account the age at development of multiple autoantibodies when evaluating risk factors for progression to a diabetes diagnosis,” said Krischner. “When the changing picture of autoantibody presentation is considered, it appears type 1 diabetes at an early age is a more aggressive form of the disease.”
