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Posted On: 08/28/2024 8:28:07 AM
Post# of 148862
Restoring hippocampal glucose metabolism rescues cognition across Alzheimer’s disease pathologies.
The authors showed that activation of indoleamine-2,3-dioxygenase 1 (IDO1) by either amyloid β or tau oligomers, two prominent Alzheimer’s disease pathological proteins, promotes the conversion of tryptophan to kynurenine, which then suppresses astrocytic glycolysis, thus reducing one of the main fuel sources for neurons. Inhibiting IDO1 rescued synaptic plasticity in vitro and improved cognition in multiple rodent models.
Per Ohm's regulator list: IDO (via IFN-y downreg) [-],
Another mechanism by which leronlimab may impact Alzheimer's....
https://www.science.org/doi/10.1126/science.abm6131
The authors showed that activation of indoleamine-2,3-dioxygenase 1 (IDO1) by either amyloid β or tau oligomers, two prominent Alzheimer’s disease pathological proteins, promotes the conversion of tryptophan to kynurenine, which then suppresses astrocytic glycolysis, thus reducing one of the main fuel sources for neurons. Inhibiting IDO1 rescued synaptic plasticity in vitro and improved cognition in multiple rodent models.
Per Ohm's regulator list: IDO (via IFN-y downreg) [-],
Another mechanism by which leronlimab may impact Alzheimer's....
https://www.science.org/doi/10.1126/science.abm6131
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