One drug (retinoic acid) seems to increase the number of lysosomes in astrocytes, while the other drug enhances the ability of the astrocytes to degrade abeta.
It will be interesting to see how it goes. We're all so used to hearing about these early results that seem so promising, but never pan out. Eventually something will.
Astrocytes studied in cell cultures and in Alzheimer's mouse models were stimulated by retinoic acid to phagocytosedestroy Aβthrough the activation of the low-density lipoprotein cholesterol receptor and triggered to subsequently degrade Aβ in lysosomes by the cholesterol-lowering drug gemfibrozil.
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Their experiments revealed that the drug combination activated a receptor called PPARα, which encouraged astrocytes to destroy the mind-damaging amyloid, the cause of plaques. PPARα stands for peroxisome proliferator-activated receptor-alpha. PPARα is a transcriptional factor that regulates the expression of genes involved in fatty acid oxidation and is also a major regulator of energy homeostasis. PPARα is critical in the elimination of amyloid beta, Aβ.