GLP-1 receptor agonists like semaglutide and liraglutide demonstrate multiple neuroprotective mechanisms in preclinical studies, including reduced protein aggregation, enhanced cellular cleanup through autophagy, improved mitochondrial function, and suppressed brain inflammation. Epidemiological data reveals reduced dementia, Parkinson's disease, and multiple sclerosis incidence among long-term users of these diabetes medications. This represents a significant development in neurodegenerative disease prevention, as these conditions have historically lacked effective disease-modifying treatments. The researchers' framing of GLP-1RAs as 'pharmacological analogues of exercise' is particularly compelling, given exercise's established but difficult-to-replicate neuroprotective benefits. Both interventions enhance insulin signaling, stabilize mitochondria, reduce inflammation, and promote synaptic plasticity through overlapping pathways. However, translation remains challenging due to uncertain brain penetration, variable patient responses, and mixed clinical trial results to date. The emergence of next-generation dual and triple hormone agonists could potentially amplify these effects, though they remain untested in neurodegeneration. This work suggests that widely-prescribed diabetes medications may offer unexpected cognitive protection, potentially transforming how we approach neurodegenerative disease prevention in aging populations already using these drugs for metabolic conditions.