Progression to Parkinson's dementia is not modulated by genetic risk variants for Alzheimer's or Parkinson's disease.

Children who experience early life stress and socioeconomic disadvantage are more likely to experience behavioral, cognitive, and physical health challenges across the lifespan (). Examination of the potential biological mediators of these developmental effects has implicated epigenetic mechanisms, such as DNA methylation, which are sensitive to adverse experiences and may also lead to stable transcriptional changes that impact physiological, neurobiological, and immune pathways with implications for health and well-being (). Variation in DNA methylation within the genome may also indicate biological aging. Increasing evidence suggests that acceleration in this molecular measure of aging is predictive of chronic disease and mortality in later life (). The present study examines the associations among prenatal stress, socioeconomic disadvantage, and epigenetic aging in newborns. We seek to examine whether biological indicators of prenatal socioeconomic disadvantage and stress are detectable at the beginning of postnatal life. Exposure to early life stress and socioeconomic disadvantage are robust predictors of worse health and well-being across multiple domains. Indeed, a recent meta-analysis found that prenatal stress robustly predicted emotional and behavioral problems in childhood, above and beyond postnatal levels of distress (). Similarly, decades of research have documented that children born into poverty are prone to demonstrate lower performance on measures of cognitive and socioemotional functioning, as well as worse physical and mental health, compared to their higher-income peers (). Experimental studies in rodent samples show that adverse exposures cause similar downstream effects. For example, offspring of rats experimentally exposed to stress during pregnancy demonstrate behavioral and cognitive changes much like those observed in human offspring, such as greater internalizing symptoms and declines in cognitive functioning (). Epigenetic modifications such as DNA methylation are one potential pathway by which these prenatal experiences may exert long-term effects. The Developmental Origins of Behavior, Health and Disease (DOBHaD) hypothesis proposed by argues that prenatal insults, such as poor nutrition, toxic stress, and environmental toxicants, can shape developing fetal systems via epigenetic pathways. For example, families residing in low-income neighborhoods tend to have reduced access to healthy foods (), and poor prenatal nutrition has subsequently been linked to epigenetic alterations in offspring (). Similarly, poorer mental health and greater levels of perceived stress during pregnancy have also been linked to alterations in infant DNA methylation, possibly explained by changes to placental regulation of glucocorticoids ().