Graphical summary of the possible connection between amylin and tau pathology in the brain and pancreas of diabetic PS19 mice. (IMAGE)
Caption
The intraperitoneal administration of amylin aggregates caused the emergence of pathogenic p-tau concomitant with a decrease in lysosomes in the pancreas of diabetic PS19 mice. Although the plasmatic amylin remained unchanged in mice at 6 months of age, we speculate that a fraction of amylin aggregates may have reached the brain during the two-week injection period (4.5 months). Peripheral amylin aggregates, through a yet unknown mechanism, contributed to the exacerbation of p-tau in the visual cortex. The increase of p-tau in the visual cortex was accompanied by decreased lysosome functionality. However, the chronological order of these events still needs to be clarified. Further research is necessary to fully understand the spatial and temporal order and the mechanisms underlying the involvement of amylin in the aggregation of tau in both the central nervous system and the periphery.
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Genes & Diseases
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