Semaglutide was supposed to quench CNS inflammation — it didn’t
The GLP-1’s anti-inflammatory effects in the periphery did not translate to the brain
If semaglutide’s failure to treat Alzheimer’s disease has a silver lining, it may be that its inability to ameliorate neuroinflammation reflects its own limits and is not a strike against neuroinflammation as a therapeutic target.
That will be little comfort to patients, who will have to wait for drug developers to deliver on that hypothesis. The result neither refutes nor supports the idea that suppressing neuroinflammation could alter the course of disease. Answers may come from therapies that act directly within the CNS, such as brain-penetrant microglial modulators or cytokine-pathway inhibitors, but they are unlikely to come soon. With so much of the field’s focus on amyloid and tau, the pipeline of neuroinflammation-targeting agents remains small and early-stage...
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