This study examined intranasal GHK peptide treatment in 5xFAD transgenic mice, a model of Alzheimer’s disease, and found that treatment attenuated both behavioral deficits and neuropathological features including amyloid-beta accumulation and neuroinflammation (animal model). The research demonstrates potential mechanisms by which GHK peptide may modulate disease-relevant pathways in Alzheimer’s disease progression, though findings are limited to preclinical mouse studies that do not directly translate to human outcomes (evidence level: animal model).