The Rhyothemis princeps Brain Externalization Project

Yesterday I watched two excellent presentations on Freidreich ataxia (still trying to use the proper nomenclature convention) from back in 2011: Notes: 5:44 frataxin is essential for muticellular eukaryotes (but not single celled organisms) frataxin is needed for the production of iron-sulfur clusters (aconitase is an important TCA enzyme that includes an iron-sulfur cluster that is particularly vulnerable to oxidation) 13:07 Indeed! & also part of the urea cycle 18:35 Reduction in frataxin leads to iron accumulation in the mitochondrion   38:26 summary of therapeutic approaches in relation to hypothetical vicious cycle in FA EPO - erythropoietin increases expression of genes related to iron utilization (lactoferrin and Wim Hof method breathing increase EPO) HDAC inhibitors increase expression of frataxin (butyrate / tributyrin are HDACi) pioglitozone increases mitochondrial biogenesis (PQQ & urolithin A do the same) I think neuroinflammation should be included as part

From a  discussion with OS on MedCram (which had gone way OT from sex differences relating to covid-19 pathology - link to discussion thread ): re: AMPK bat genetics - not much yet, but there's this one Positive Selection of Cereblon Modified Function Including Its E3 Ubiquitin Ligase Activity and Binding Efficiency With AMPK - https://pubmed.ncbi.nlm.nih.gov/30836149/ Note the same modification is present in both bats and rodents. Hamsters do seem to have some protection from oxidative stress, but they are not particularly long-lived as are bats. They are what's termed 'r selected' - with a life history characterized by high reproductive rate and short life-span. Here's an article that points out that oxidative stress defenses may be tissue specific and that hamsters may not have as much protection in the brain: Oxidative Damage Does Not Occur in Striped Hamsters Raising Natural and Experimentally Increased Litter Size - https://www.ncbi.