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Relevant studies have found that exendin-4 could mediate the neuroprotective effect on g- aminobutyric acid neurons in the piriform cortex and striatum and play a neuroprotective role in a cAMP/PKA- and PI3K/ AKT-dependent manner after stroke (84,85)

The COX and LOX pathways are the primary routes for metabolizing AA into inflammatory mediators and breaking it down into leukotrienes, prostaglandins, and some peroxides [58]

For other neurodegenerative diseases like ALS and MS, the evidence for the therapeutic value of KD or KS are limited, yet promising

Whether such a low dose provides meaningful metabolic benefit is questionable

And even then, the results take time, so judge it over months, not days