Alzheimer’s disease (AD) is a multifactorial neurodegenerative disorder characterized by progressive cognitive decline and neuronal loss. In recent years, the AGE-RAGE (advanced glycation end-products/receptor for AGEs) signaling pathway has emerged as a key contributor to AD pathogenesis, amplifying oxidative stress, mitochondrial dysfunction, neuroinflammation, and impaired glucose metabolism. This review combines a bibliometric analysis of recent literature (2016–2024) with a critical discussion of molecular mechanisms linking AGE-RAGE activity to classical AD hallmarks, including amyloid-beta accumulation and tau hyperphosphorylation. The metabolic overlap between AD and type 2 diabetes mellitus further supports the hypothesis that AGE-related stress contributes to disease onset and progression. Several natural and pharmacological compounds—including antioxidants, antiglycation agents, and metabolic modulators—have shown promise in targeting this axis. Notably, agents such as 1,8-cineole, trigonelline, and benfotiamine demonstrate neuroprotective effects by reducing AGE accumulation and oxidative damage. This review proposes that therapeutic strategies integrating AGE-RAGE inhibition, metabolic regulation, and oxidative stress control may offer more effective approaches than single-target interventions. The findings highlight the need for multi-targeted, personalized therapies to address the complex pathological landscape of AD and improve long-term outcomes.
Staudt et al. (Tue,) studied this question.
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