In adults <60 with subjectivecognitive decline (SCD), co-occurringsymptoms (anxiety, depression, fatigue, sleep disturbance, pain) maysignal early neurodegeneration, and identifying their epigenetic correlatesmay reveal biological pathwaysunderlying symptom-related cognitivevulnerability. SCD adults <60 were grouped ashigh (HSB, n=18) vs. low (LSB, n=31)symptom burden. Saliva DNA wasassayed via IlluminaMethylationEPIC; age acceleration(AA) was assessed by HorvathAAand GrimAA, and genome-wide CpGmethylation compared betweengroups. Among adults aged <60years with SCD, high multidimensional symptom burden was associated with PCDH19hypermethylation, whereas global epigenetic aging indices (HorvathAAand GrimAA) were not significantly different. These finding Suggest that symptom burden in younger adults with SCD may be better reflected by gene-specific epigenetic alterations than by accelerated epigenetic aging. Future studies with larger samples and longitudinal follow-up should validate the PCDH19 methylation signals and evaluate its potential as a biomarker for symptom-related cognitive vulnerability.