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The paper concludes by proposing a unified mechanism whereby BBB dysfunction contributes to neurodegenerative disorders, highlights potential BBB-focused therapeutic strategies and targets, and outlines lessons learned and future research directions

Gene expression and cellular regulation Epithalon's broader cellular effects: Modulates over 100 genes related to aging and longevity Upregulates genes involved in DNA repair Downregulates pro-inflammatory genes Influences antioxidant enzyme production Affects genes controlling cellular metabolism Key gene expression changes: Upregulated (increased): Telomerase (hTERT gene) Antioxidant enzymes (SOD, catalase, glutathione peroxidase) DNA repair enzymes Cell survival genes (Bcl-2 family) Collagen synthesis genes (in some tissues) Downregulated (decreased): Pro-inflammatory cytokines (IL-6, TNF-alpha) Pro-apoptotic genes (excessive cell death) Senescence-associated genes Oxidative stress markers Cellular pathways affected: Mitochondrial function : Improved energy production Autophagy : Enhanced cellular cleanup Protein synthesis : Better quality proteins Immune regulation : Balanced response Hormone production : More youthful levels Why gene regulation matters: Aging partly driven by gene expression changes Restoring youthful gene patterns reverses age-related decline Multiple pathways = comprehensive anti-aging effect Not just one mechanism (telomeres) but systemic optimization Similar comprehensive effects seen with other anti-aging peptides like GHK-Cu and thymalin