Neurologic Complications of Poverty: the Associations Between Poverty as a Social Determinant of Health and Adverse Neurologic Outcomes.

PURPOSE OF REVIEW: Increasing attention has been paid in recent decades to social determinants of health as a risk factor for disease development and disease severity. While traditionally heart disease, family history, lipid profile, and tobacco use have all been associated with increased risk of neurological disease, numerous studies now show that the influence of poverty may be just as strong a risk factor. This study summarizes the recent literature on poverty as it contributes to neurological disease. RECENT FINDINGS: Children growing up in poverty have increased risk for cognitive deficits and behavioral disorders as reported by Noble et al. (Dev Sci. 9(6):642-54, 2006) and Farah et al. (Brain Res. 1110(1):166-74, 2006) as well as worse outcomes when it comes to epilepsy management and disease course as discussed by Camfield et al. (Epilepsia. 57(11):1826-33, 2016). In adulthood, as the number of social determinants of health increases, the incidence of stroke and severe stroke increases significantly as reported by Reshetnyak et al. (Stroke. 51:2445-53, 2020) as does exposure to neurologically significant infectious diseases and incidence of dementia as reported by Sumilo et al. (Rev Med Virol. 18(2):81-95, 2008) and Zuelsdorff et al. (Alzheimer's Dement. 6(1):e12039, 2020). Social determinants of health including poverty should be considered a risk factor for disease. More attention is needed from clinicians as well as from a public health perspective to address this disparity.

Copper: toxicological relevance and mechanisms.

Copper (Cu) is a vital mineral essential for many biological processes. The vast majority of all Cu in healthy humans is associated with enzyme prosthetic groups or bound to proteins. Cu homeostasis is tightly regulated through a complex system of Cu transporters and chaperone proteins. Excess or toxicity of Cu, which is associated with the pathogenesis of hepatic disorder, neurodegenerative changes and other disease conditions, can occur when Cu homeostasis is disrupted. The capacity to initiate oxidative damage is most commonly attributed to Cu-induced cellular toxicity. Recently, altered cellular events, including lipid metabolism, gene expression, alpha-synuclein aggregation, activation of acidic sphingomyelinase and release of ceramide, and temporal and spatial distribution of Cu in hepatocytes, as well as Cu-protein interaction in the nerve system, have been suggested to play a role in Cu toxicity. However, whether these changes are independent of, or secondary to, an altered cellular redox state of Cu remain to be elucidated.