The 81st Annual Meeting of the American Association of Physical Anthropologists (2012)

The role of glia in human brain evolution


1Department of Anthropology, Emory University, 2Division of Neuropharmacology and Neurological Diseases, Yerkes National Primate Research Center, Emory University, 3Center for Translational Social Neuroscience, Yerkes National Primate Research Center, Emory University

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Human brain evolution presents a striking paradox. Modern humans have especially large brains with unusually high metabolic activity per gram of tissue. High levels of oxidative metabolism imply high levels of reactive oxygen species production, resulting in increased tissue damage. Despite this, humans live longer than any other primate and many humans maintain functional cognitive acuity for 80 years or more. Comparative genomic studies suggest that humans evolved patterns of gene expression to support high levels of synaptic activity and plasticity (Preuss et al. 2004). These studies also demonstrate an evolutionary up-regulation in the expression of genes involved in oligodendrocyte function and myelin formation in the human lineage relative to the ape lineage. The molecular consequences of genetic changes in the white matter of the brain may be directly relevant to the uniquely human features of cognition, longevity and neurodegeneration. We conducted histological studies of myelin-related proteins and activated glial cells in white matter in monkeys, apes, and humans. Our results indicate increased expression of some myelin-related proteins in human brains relative to ape and macaque brains, as well as species differences in patterns of microglia and astrocyte activation. Factors such as age and sex also play a role. These findings suggest that the balance of regenerative and destructive forces in the brain shifted in human evolution either by enhancing myelin regeneration by oligodendrocytes and/or by diminishing degenerative processes mediated by astrocytes and microglia.

This study was funded by the Mathers Foundation Grant #00016382.

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