Cognitive Neurogenetics

As a component of investigating the biological bases of reasoning our research seeks to identify pathways of effect through which genetic variations influence reasoning-related cognitive functions (Fossella et al., 2006; Green, Munafo, et al., 2008; Green & Dunbar, 2012; Green, Kraemer, et al., 2013; Green et al., 2014). While “cognitive neurogenetic” research of this kind shows strong potential, this emerging field has not yet outgrown serious theoretical and interpretive hazards.

One focus of our research is to identify sources of these hazards. In critical analyses of recent research, we have outlined methodological considerations for the “intermediate phenotype approach,” and emphasized statistical and paradigmatic strategies to ensure that results can be meaningfully interpreted (Green, Munafo et al., 2008; Green & Dunbar, 2012). The long-term goal of this work, in combination with our primary research lines described above, is to develop a stronger vertical integration of data on human reasoning at cognitive, neural, and genetic levels. Toward this goal, we have developed and tested gene-brain-cognition effect pathways that integrate data at the genetic, neural, and behavioral levels within a single directional model. We have used this approach to show that activity in four frontal brain regions mediates effects of a dopamine system-related gene on executive attention and IQ (Green, Kraemer et al., 2013).

Other work has challenged the assumption that COMT genotypes assumed to yield greater neural “efficiency” actually yield performance advantages at highly demanding levels of common working memory tasks (Ihne et al., 2016). In collaboration with Dr. G. William Rebeck in the Department of Neuroscience at Georgetown, we have conducted a series of studies investigating the effects of genetic Alzheimer’s risk factors on brain structures and functions that support reasoning and executive function. This work has further demonstrated the efficacy of gene-brain-cognition modeling, and has generally supported an antagonistic pleiotropy account of Alzheimer’s genetic risk whereby genetic variants that confer risk late in life actually confer neurocognitive advantages in young people (Green et al., 2014; DiBattista et al., 2014; Stevens et al., 2014). New research in this area is exploring whether genetic Alzheimer’s risk factors affect spatial neurocognition in young participants.

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