Epigenetic modifications of chromatin structure provide a mechanistic interface for gene-environment interactions that impact the individualization of health trajectories across the lifespan. A growing body of research indicates that dysfunctional epigenetic regulation contributes to poor cognitive outcomes among aged populations. Here we review neuroepigenetic research as it relates to cognitive aging, focusing specifically on memory function mediated by the hippocampal system. Recent work that differentiates epigenetic contributions to chronological aging from influences on mindspan, or the preservation of normal cognitive abilities across the lifespan, is also highlighted. Together, current evidence indicates that while age-related memory impairment is associated with dysfunction in the coordinated regulation of chromatin modification, animal models that show individual differences in cognitive outcome underscore the enormous mechanistic complexity that surrounds epigenetic dynamics in the aged hippocampus.Cognitive decline, especially memory loss, is one of the most prevalent and feared consequences of growing older. In the United States it is expected that by 2050, 12% of people over the age of 65 will suffer from moderate-to-severe memory impairment (Federal Interagency Forum on Aging-Related Statistics: Older Americans Update 2004). Understanding the neural basis of cognitive decline is all the more pressing in light of national demographic trends highlighting the rapidly expanding elderly population, with the number of people aged 65 and older projected to increase from 43 million to more than 83 million over the next four decades (Ortman et al. 2014). Alongside a focus on negative outcomes, there is increasing recognition that memory decline is not an inevitable consequence of aging as some older adults maintain normal memory abilities across the lifespan. Identifying the neurobiological mechanisms that impact differential cognitive outcomes with age is critical. In this context, research exploring the biological substrates that drive individual healthspan trajectories from early development through old age can provide valuable insight into the brain mechanisms that influence mindspan.A life course perspective emphasizes that environmental and experiential factors operate throughout life to potently influence the biological mechanisms that dictate the arc of an individual's health trajectory (for review, see Halfon et al. 2014). An emerging theme is that age alone is only a coarse predictor of health outcome, and current efforts are focused on disentangling chronological age effects from other determinants of functional outcomes in the elderly. Epigenetic modifications of the genome have gained attention in this context since they allow for genomic plasticity in post-mitotic cells and provide a means by which environment and experience interface with gene transcription to impact biological functions across the lifespan. This plasticity is crucial for adaptation and resilience in the face of environmenta...