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TL;DR
This preclinical study used molecular, cellular, and mouse models to investigate if the antipsychotic amisulpride interacts with the glucose transporter GLUT1 at the blood-brain barrier, which may be relevant to Alzheimer's disease.
PLOS ONE · 18 authors, 9 centres
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This preclinical study used molecular, cellular, and mouse models to investigate if the antipsychotic amisulpride interacts with the glucose transporter GLUT1 at the blood-brain barrier, which may be relevant to Alzheimer's disease.
The study combined in silico, in vitro, and in vivo methods to explore amisulpride's interaction with GLUT1 and blood-brain barrier (BBB) transport in Alzheimer's disease (AD). A literature review and molecular docking suggested amisulpride interacts with GLUT1. In vitro assays with hCMEC/D3 cells showed no functional inhibition of glucose transport by amisulpride. In situ brain perfusion in 5xFAD mice and wild-type mice found no significant difference in brain uptake of amisulpride. Transmission electron microscopy revealed brain capillary degeneration in a human AD sample. Western blot analysis showed no difference in GLUT1 expression between mouse models but found decreased P-glycoprotein, but not GLUT1, in human AD capillaries. Limitations include the use of a cell line and a mouse model that may not fully replicate human AD, and the inability to detect a direct functional interaction in vitro. The findings suggest amisulpride interacts with GLUT1 but do not confirm altered BBB transport in AD models, though they support the need for caution with antipsychotics in AD.