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In symptomatic AD, nuclear translocation of NRF2 is inhibited, preventing its transcriptional function ( Furthermore, upregulation in REST reduces astrocyte reactivity through repression of inflammatory markers that segregate astrocytes into a reactive subpopulation, thus preventing neuroinflammation-induced reactive cells from populating the brain and exerting neurotoxic effects in human induced pluripotent stem cell (hiPSC)-derived astrocytes from patients with Down syndrome, a condition associated with early-onset AD (Huang et al., 2025)
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The mechanisms by which released FAs promote insulin secretion is likely through the sensing of FAs by GPR40 receptor found on the surface of beta cells (153)
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