111. More Research to Solve Alzheimer’s, EV Energy Sharing, Tesla Virtual Power Plants

Summary: NEWS: Sugar-studded protein is key to an Alzheimer's cure | The Brighter Side (01:38) In a bit of “reverse engineering” research using brain tissues from five people who died with Alzheimer’s disease, Johns Hopkins Medicine researchers say they discovered that a special sugar molecule could play a key role in the development of Alzheimer’s disease. This could indicate the molecule, known as a glycan, to be used as an early diagnostic test. And opens a way to perhaps prevention of the disease Cleaning up the disease-causing forms of amyloid and tau is the job of the brain’s immune cells, called microglia. Earlier studies found that when cleanup is impaired, Alzheimer’s disease is more likely to occur.  Thought to be caused by an overabundance of a receptor on the microglia cells, called CD33. Past studies by the researchers showed that for CD33, these “connector” molecules are special sugars.These molecules are ferried around the cell by specialized proteins that help them find their appropriate receptors.  The protein-glycan combination is called a glycoprotein.  The researchers, to find out more about the glycoproteins, obtained brain tissue from five people who died of Alzheimer’s disease and from five people.Among the many thousands of glycoproteins they gathered from the brain tissues, only one connected to CD33. What was this mysterious glycoprotein?The researchers determined the protein component’s identity by taking its “fingerprint” using mass spectroscopy, which identifies protein building blocks. Then they compared the molecular makeup of the protein with a database of known protein structures. The research team was able to conclude the protein portion of the glycoprotein was receptor tyrosine phosphatase (RPTP) zeta. Further experiments showed that the brain tissue of the five people who died with Alzheimer’s disease had more than twice as much RPTP zeta S3L as the donors who did not have the disease. Implying that this glycoprotein may be connecting with more CD33 receptors than a healthy brain, limiting the brain’s ability to clean up harmful proteins. Gonzalez-Gil Alvarenga, Ph.D., first author on the study stated:“Identifying this unique glycoprotein provides a step toward finding new drug targets and potentially early diagnostics for Alzheimer’s disease.”   A Surprising Link Between Immune System and Hair Growth | Neuroscience News (07:36) Salk scientists have uncovered an unexpected molecular target of a common treatment for alopecia, a condition in which a person’s immune system attacks their own hair follicles, causing hair loss. Corresponding author of the study, Ye Zheng, associate professor in Salk’s NOMIS Center for Immunobiology and Microbial Pathogenesis, stated:“For the longest time, regulatory T cells have been studied for how they decrease excessive immune reactions in autoimmune diseases … Now we’ve identified the upstream hormonal signal and downstream growth factor that actually promote hair growth and regeneration completely separate from suppressing immune response.” Initially the researchers were interested in researching the roles of regulatory T cells and glucocorticoid hormones in autoimmune diseases.They did not function together to play a significant role in any of these conditions.  Thought they’d have more luck looking at environments where regulatory T cells expressed particularly high levels of glucocorticoid receptors The glucocorticoid receptor (GR, or GCR) also known as NR3C1 (nuclear receptor subfamily 3, group C, member 1) is the receptor to which cortisol and other glucocorticoids bind. The scientists induced hair loss in normal mice and mice lacking glucocorticoid receptors in their regulatory T cells.After two weeks, the researchers saw the normal mice grew their hair back, while the ones lacking the receptors struggled to grow it back The findings suggested that some sort of communication must be occurring between regulatory T cells and hair follicle ste