The Rhyothemis princeps Brain Externalization Project

Modern Healthspan released a video on an article that reports that shikimic acid reduced markers of  UV light induced cellular senescence in cultured dermal fibroblasts, increased SIRT1 activity and restored proteostasis . As MH suggests in the video, these findings could have much broader implications. Video: https://youtu.be/m_qaZSsFiT8 Research article:  Martinez-Gutierrez et al. (2021) https://www.aging-us.com/article/203010/text "SA reverted misfolded protein accumulation upon senescence, an effect that was abrogated by EX-527. Consistently, SA induced an increase in the levels of the chaperone BiP, resulting in a downregulation of unfolded protein response (UPR) signaling and UPR-dependent autophagy, avoiding their abnormal hyperactivation during senescence. SA did not directly activate SIRT1 in vitro, suggesting that SIRT1 is a downstream effector of SA signaling specifically in the response to cellular senescence. Our study not only uncovers a shikimic acid/SIRT1 signaling

Someone on a forum asked why iNOS inhibitors (e.g., agmatine, anatabine) would be beneficial and my reply follows: Too much NO generates peroxyynitrite and can cause nitrosative and oxidative stress, causing production of nitrated/oxidized alpha synuclein and oxidized dopamine. NO generated by iNOS in glial cells is particularly problematic for neurons. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3408780/ This is in contrast with NO generated by the endothelium during exercise, which acts on the endothelium (autocrine signalling) which in turn produces good things like BDNF (the vascular endothelium can be thought of as an endocrine organ). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2791344/ https://youtu.be/lhZZS6_-Cg4 There are lots of studies on iNOS inhibitors in models of Parkinson's and other neurodegenerative disease. https://pubmed.ncbi.nlm.nih.gov/31192483/ Tobacco use and Solanaceae vegetable consumption are associated with reduced risk of PD. If causal, the relations