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Increased cortical expression of two synaptogenic thrombospondins in human brain evolution
Mario Cáceres1, Carolyn Suwyn, Marcelia Maddox
1Division of Neuroscience and Center for Behavioral Neuroscience, Yerkes National Primate Research Center, Emory University, 954 Gatewood Road, Atlanta, GA 30329, USA.
Cerebral Cortex (New York, N.Y. : 1991)
|December 22, 2006
Summary
Thrombospondin genes (THBS4 and THBS2) show increased expression in human brain evolution, particularly in the cerebral cortex. This may influence human cognition and neurodegenerative disease vulnerability.
Area of Science:
- Neuroscience
- Evolutionary Biology
- Genetics
Background:
- Thrombospondins are extracellular proteins crucial for synaptogenesis and neurite growth.
- Previous studies indicated thrombospondin 4 (THBS4) upregulation during human brain evolution.
Purpose of the Study:
- To investigate differential expression of thrombospondin genes (THBS4 and THBS2) in the human brain compared to non-human primates.
- To characterize the cellular and regional distribution of thrombospondin expression in the human brain during evolution.
Main Methods:
- Quantitative analysis of THBS4 and THBS2 mRNA and protein levels in adult human, chimpanzee, and macaque brain samples.
- Histological examination and immunohistochemistry to determine cellular localization and protein distribution.
Main Results:
- Humans exhibit significantly higher THBS4 and THBS2 mRNA and protein levels in the cerebral cortex compared to chimpanzees and macaques.
- Differential expression was primarily observed in the forebrain, with similar levels in the cerebellum and non-brain tissues.
- THBS4 expression in humans was prominent in the cortical neuropil and associated with beta-amyloid plaques in Alzheimer's disease.
Conclusions:
- Increased thrombospondin expression in the human brain may underlie enhanced synaptic organization and plasticity, contributing to human cognitive abilities.
- Elevated thrombospondin levels could also be linked to human susceptibility to neurodegenerative diseases like Alzheimer's.
