A possible role for glucose transporter inhibition in the genistein-induced amelioration of a high glucose C. elegans Alzheimer disease model.

Abstract

Wang and colleagues (Wang et al., Free Rad Biol Med, 242 (2026) 167-187) have found in in silico and in vitro experiments, that multifaceted molecule genistein inhibits many of the detrimental effects of high glucose in a C. elegans-based Alzheimer disease model that expresses β-amyloid in a temperature-dependent fashion. Genistein inhibits, amongst many other pathophysiogical parameters, the glucose-induced aggregation of β-amyloid. While these findings are of interest, a few possible explanations are missing. Here, we hypothesize that genistein may inhibit some of the high glucose effects through its previously described inhibitory interaction with glucose transporters.