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Friday, July 20, 2018 8:57:55 PM
it is my opinion that the Sigma-1 concept is over-emphasized as the main MOA of A2-73. that MOA is certainly important but i believe and have tried to show with my posting of abstracts that Ca2+ homeostsis is the most important MOA of A2-73. yet to be proven but still if it can be shown..well..
Ca2+ dyshomeostasis, ER stress and defects in lipid metabolism and autophagy. Intriguingly, many of these cellular processes are perturbed in neurodegenerative diseases. Furthermore, increasing evidence highlights that ER–mitochondria signaling contributes to these diseases, including Parkinson’s disease (PD). PD is the second most common neurodegenerative disorder, for which effective mechanism-based treatments remain elusive. Several PD-related proteins localize at mitochondria or MAM and have been shown to participate in ER–mitochondria signaling regulation. Likewise, PD-related mutations have been shown to damage this signaling. Could ER–mitochondria associations be the link between pathogenic mechanisms involved in PD, providing a common mechanism? Would this provide a pharmacological target for treating this devastating disease?
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5832754/
from the same article this is the linking i am hoping can be deciphered;
These include alterations in Ca2+ homeostasis, cellular proteostasis, axonal transport, mitochondrial function, and neuroinflammation3. Consequently, one of the difficulties in deciphering PD-related toxicity consists of linking these apparently diverse pathological changes to a common disease pathway.
lipid function is also IMO very important as stated in first quote and if curious folks are interested see my recent posts for a phase 3 CV outcomes study that results will be released in weeks. GL
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