This week on Lifespan News, Brent Nally discusses thyroid organoids for potential human use, a human trial showing that clearing amyloid plaques slows mental decline, reduced NMN as a NAD+ precursor, shortened telomeres and kidney fibrosis, and our STSTW episode on meditation.
We’ve all heard of organs, and we all have many organs inside of us. But have you heard of organoids? Stay tuned to find out what organoids are and how organoids could help improve healthspan and lifespan in humans in the future. We’ll have this story plus four other stories in this episode of Lifespan News.
Welcome to Lifespan News on x10, your source for longevity science updates. I’m your host, Brent Nally. If you missed our last episode, then you can watch it by clicking the card above. We encourage you to check the description below for links to these stories.
Continuing with our first story, thyroid organoids have been created from human tissue. This innovative approach may one day lead to thyroid replacement. Researchers have developed organoids to replace thyroid function, which could help treat hypothyroidism. Hypothyroidism is one of the most common afflictions around the world, and it increases with age. The current treatment doesn’t work fully in 5 to 10 percent of sufferers. The current pharmaceutical approach to hypothyroidism is to simply replace at least one of the hormones that the thyroid produces. However, the researchers of this study have created small artificial organs known as organoids that live within tissue and create such hormones themselves. The researchers created organoids from human and mouse cells and showed that they had thyroid characteristics and were not expressing tumor-related genes, which is a common problem in regenerative medicine. However, the organoids also didn’t produce enough hormones to help thyroid-damaged mice. The researchers present this as a proof of principle. If the researcher’s approach can go through the development and human clinical trial process, the resulting therapy could potentially function exactly as a human thyroid does, thus removing the need for pharmaceutically created hormones.
For our next story, a human trial suggests clearing plaques slows mental decline. At the 15th International Conference on Alzheimer’s and Parkinson’s Diseases, Dr. Mark Mintun of Eli Lilly presented data on the performance of the anti-amyloid drug donanemab. Eli Lilly’s Phase 2 clinical trial data for its anti-amyloid antibody donanemab reached its endpoint. While the patients did not get better, the administration of donanemab appeared to slow decline by an average of 32 percent in combined assessment of cognitive and functional decline. The results show that donanemab was able to remove the plaques associated with Alzheimer’s in the majority of trial participants while also reducing the accumulation rate of neurofibrillary tangles in the frontal cortex and other regions. The results of the trial suggest that treatments aimed at amyloid can slow cognitive decline and modify the progression of Alzheimer’s, but the fact that the treatment didn’t improve or reverse conditions could indicate that targeting amyloid alone isn’t enough. It might be that a combination of anti-amyloid and anti-tau drugs is needed for optimal treatment. Donanemab is now being tested in the phase 3 Trailblazer trial, due to run until 2024.
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Reduced nicotinamide mononucleotide is a new NAD+ precursor. A new study suggests that reduced nicotinamide mononucleotide, or NMNH, is a potent nicotinamide adenine dinucleotide, or NAD, precursor molecule. NMNH could serve as an alternative to nicotinamide mononucleotide, or NMN, and nicotinamide riboside, or NR, precursors which are currently sold as dietary supplements. NAD, is an important area of focus for aging research. NAD supports DNA repair, activates sirtuins that are known as the longevity genes, facilitates processes such as glycolysis and the citric acid cycle, takes part in redox reactions, and allows the electron transport chain inside the mitochondria to function. The downstream activity of NAD supports hundreds of enzymatic reactions and regulates many key processes in cells. As we age, our levels of NAD declines significantly, so the restoration of NAD levels has been the focus of significant research efforts in the last few years. In the new study, researchers developed a way of creating and purifying NMNH at scale and explored its role in NAD biology. Study results demonstrate that NMNH is efficiently processed into NAD in cells, and this did not involve enzymes known to be important for other precursors. NMNH treatment in mice was able to raise NAD levels in their blood but also in multiple tissues, including the kidneys, and to a higher level than NMN at a similar concentration. So NMNH may prove to be a new precursor for those looking for an NAD boost. The researchers focus on scale and the potential lower dosage could make NMNH cheaper than existing alternatives.
Moving on, shortened telomeres increase kidney fibrosis rates in mice. Telomere shortening is one of the primary hallmarks of aging. Tissues with short or dysfunctional telomeres can lose their regenerative capacity and become fibrotic. Kidney fibrosis becomes more common with age, with 11 percent of people of 65 having stage 3 chronic kidney disease. Researchers in Spain generated a mouse model which could be used to investigate the link between shortened telomeres and kidney fibrosis. The researchers accomplished this by dosing mice with folic acid, a chemical that causes kidney damage. By testing varying doses, the researchers found a folic acid level which caused kidney fibrosis in telomerase mutants but not in wild type mice. These mice showed all the hallmarks of human kidney disease, making these mice a potentially valuable model for studying kidney fibrosis and testing therapies. The team also developed a second mouse model by deleting the Trf1 gene, which is part of the shelterin complex that protects telomeres. These mutants developed kidney fibrosis without folic acid treatment. In both mouse models, fibrosis was accompanied by epithelial cells losing their identity and becoming mesenchymal cells, which is a process known as epithelial-to-mesenchymal transition, or EMT. Consistent with this, the expression of EMT-associated genes increased with fibrosis in both new models. EMT is part of the normal wound healing and regeneration processes, but it’s also active in cancer and fibrotic diseases. These models could thus be invaluable in teasing apart the molecular underpinnings linking EMT and age-related diseases. These offer scientists tools to investigate how telomere shortening causes fibrosis, digging into the regulation of EMT. Understanding these processes may reveal mechanisms linking aging and telomeres not only with fibrosis but with other conditions, such as cancer. This story will be the topic of The Journal Club on LEAF’s Facebook page on Wednesday March 31st, 2021 at noon Eastern Time so we hope to see you there!
For our final story, the latest Science to Save the World episode discusses what meditation does in the brain and how it can be used to increase mindfulness. This may possibly alter people’s attitudes towards issues in their lives. Science is showing that meditation can build desirable mental traits by inducing changes in the brain. Neuroplasticity is the brain’s ability to grow and reorganize in response to experience. Researchers are trying to understand this process so we can use that knowledge to be healthier and happier. The next episode of Science to Save the World will dig further into what meditation does to the brain and how it could help address global issues like climate change and inequality.
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