Background/Objectives: Gliomas arise from distinct subgroups driven by different genetic alterations. Gain-of-function mutations in isocitrate dehydrogenase 1/2 (IDH1/2) are frequent in a subset of gliomas and are associated with improved survival compared with wild-type tumors. IDH-mutant gliomas can be classified as having the CpG island methylator phenotype (G-CIMP), which is characterized by widespread epigenetic changes associated with IDH1 mutations. G-CIMP-based stratification provides an added improvement in glioma classification when considered alongside grade and histology. Despite the success of G-CIMP-based stratification in predicting outcome in some patients, it does not fully account for non-responders, largely due to heterogeneity within G-CIMP gliomas. Methods: Using a The Cancer Genome Atlas (TCGA) glioblastoma, IDH-wildtype discovery cohort, we identified gene-level DNA methylation and expression patterns associated with clinical outcomes, including epigenetically regulated genes such as TUBB2A and TM4SF1. Results: In an independent TCGA diffuse glioma validation cohort enriched for IDH-mutant tumors, canonical IDH-defined G-CIMP classification was applied, and promoter methylation of TUBB2A and TM4SF1 showed significant associations with overall survival. Conclusions: These findings highlight molecular heterogeneity within IDH-defined G-CIMP gliomas and demonstrate that gene-specific methylation events can refine prognostic stratification beyond IDH status alone.

A steady increase in the elderly demographic, particularly those 85+ in age, has given rise to an elevation in global prevalence of neurodegenerative disorders, such as Alzheimer's and Parkinson's diseases, and underscores an urgent need for novel, preventive, and disease-modifying strategies. Marine ecosystems represent a prolific source of bioactive compounds, among which xanthophyll carotenoids—oxygenated derivatives including astaxanthin, fucoxanthin, and canthaxanthin—have emerged as compelling candidates for neuroprotection. These compounds exhibit superior bioavailability and blood-brain barrier permeability compared to hydrocarbon carotenoids, attributed to their polar functional groups. Their potent bioactivity stems from a multifaceted ability to modulate core pathological processes: directly quenching reactive oxygen species, activating the Nrf2-mediated antioxidant response, inhibiting NF-κB-driven neuroinflammation, and interfering with the aggregation of toxic proteins like amyloid-β and α-synuclein. This review evaluates the preclinical and clinical evidence supporting the neuroprotective potential of these three marine xanthophylls. Astaxanthin demonstrates the most robust and extensive evidence base, from cellular models to human cognitive trials. Fucoxanthin shows parallel promise with unique effects on mitochondrial biogenesis, while canthaxanthin remains significantly understudied despite its strong antioxidant profile. We further discuss the translational challenges of bioavailability and formulation, highlighting innovative delivery systems, and propose future research directions to harness these marine-derived compounds for promoting brain health and mitigating age-related cognitive decline.