Researchers explored the biological mechanisms by which exercise-induced irisin attenuates amyloid-beta pathology in Alzheimer’s disease.
By Pooja Toshniwal PahariaSep 8 2023Reviewed by Danielle Ellis, B.Sc. In a recent study published in Neuron, researchers explored the biological mechanisms by which exercise-induced irisin attenuates amyloid-beta pathology in Alzheimer’s disease .
A three-dimensional human brain cell culture model of AD with robust Aβ generation was used, followed by a tau pathology model. Irisin was administered to differentiated ReN cells that expressed familial AD-related APPSwedish/London amino acid substitutions or presenilin-1 and APPSwedish/London amino acid substitutions for two weeks at concentrations of 5.0 as well as 500 nanograms per mL.
The action of sacubitril, a neprilysin inhibitor, was examined in conditioned media comprising three-dimensional cultures. Human-induced pluripotent stem-cell-derived astrocyte cells were treated with irisin to see if they were the source of the irisin-induced rise in secreted NEP. In irisin-treated cells, the levels of astrocyte reactivity markers, S100 calcium-binding protein B , and GFAP were measured. Single-cell ribonucleic acid sequencing was performed to examine irisin-induced cell-specific transcriptome alterations,
In five-week three-dimensional-AD cultures, irisin treatment did not enhance LDH release, showing that the irisin-induced Aβ reduction did not occur from cell death. Instead, it lowered LDH secretion at 500 nanograms per mL in five-week three-dimensional-AD cells at the time of endogenous loss of cells, showing neuroprotective benefits.
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