Racial-group differences in IQ in the Minnesota Transracial Adoption Study: A reply to Levin and

The etiology of racial differences in intelligence and achievement is one of the most heated areas of social science research. In this article, we respond to criticisms by Levin and Lynn of our 1992 follow-up study of IQ and achievement in a sample of transracial adoptees and their families, in particular to their assertion that our results provide strong support for a genetic etiology underlying racial differences in measured intelligence. In that follow-up, as well as in publications from the original study In this article, we address a number of issues raised in Levin's and Lynn's critiques, including the magnitude of adoptee racial-group differences in IQ and achievement, the inclusion of white and Asian/Indian adoptee groups in such analyses, the confounding of important early environmental influences with race differences, the confusion of withingroup and between-group influences on IQ, the regional U.S. differences in AfricanAmerican norms for IQ and achievement, the effects of renormed IQ tests on adoptee group differences, and the nature of the available evidence regarding a genetic hypothesis for racial differences in intelligence. We argue that, contrary to Levin's and Lynn's assertions, results from the Minnesota Transracial Adoption Study provide little or no conclusive evidence for genetic influences underlying racial differences in intelligence and achievement. Racial-group differences in intelligence and achievement are often observed but seldom explained to anyone's satisfaction. A variety of etiological speculations have been offered to explain such differences. These have included environmental factors, such as the pervasive effects of poverty The authors wish to acknowledge the helpful comments of an anonymous reviewer. Correspondence and requests for reprints should be sent t

Gi/o-protein coupled receptors in the aging brain

Cells translate extracellular signals to regulate processes such as differentiation, metabolism and proliferation, via transmembranar receptors. G protein-coupled receptors (GPCRs) belong to the largest family of transmembrane receptors, with over 800 members in the human species. Given the variety of key physiological functions regulated by GPCRs, these are main targets of existing drugs. During normal aging, alterations in the expression and activity of GPCRs have been observed. The central nervous system (CNS) is particularly affected by these alterations, which results in decreased brain functions, impaired neuroregeneration, and increased vulnerability to neuropathologies, such as Alzheimer's and Parkinson diseases. GPCRs signal via heterotrimeric G proteins, such as Go, the most abundant heterotrimeric G protein in CNS. We here review age-induced effects of GPCR signaling via the Gi/o subfamily at the CNS. During the aging process, a reduction in protein density is observed for almost half of the Gi/o-coupled GPCRs, particularly in age-vulnerable regions such as the frontal cortex, hippocampus, substantia nigra and striatum. Gi/o levels also tend to decrease with aging, particularly in regions such as the frontal cortex. Alterations in the expression and activity of GPCRs and coupled G proteins result from altered proteostasis, peroxidation of membranar lipids and age-associated neuronal degeneration and death, and have impact on aging hallmarks and age-related neuropathologies. Further, due to oligomerization of GPCRs at the membrane and their cooperative signaling, down-regulation of a specific Gi/o-coupled GPCR may affect signaling and drug targeting of other types/subtypes of GPCRs with which it dimerizes. Gi/o-coupled GPCRs receptorsomes are thus the focus of more effective therapeutic drugs aiming to prevent or revert the decline in brain functions and increased risk of neuropathologies at advanced ages.This work was supported by Fundação para a Ciência e Tecnologia, Centro 2020 and Portugal 2020, the COMPETE program, QREN, and the European Union (FEDER program) via the GoBack project (PTDC/CVT-CVT/32261/2017), the pAGE program (Centro-01-0145-FEDER-000003), and Institute for Biomedicine iBiMED (UID/BIM/04501/2013; UID/BIM/04501/2019).publishe