5 August 2008

The High Cost Of Intelligence

by Kate Melville

The metabolic changes responsible for the evolution of human cognitive abilities indicate that the brain may have been pushed to the limit of its capabilities and that schizophrenia may be one of the costly by-products of this evolutionary leap, say scientists in the journal Genome Biology .

The idea that some neurological diseases are the by-products of increases in metabolic capacity and brain size has been suggested previously, but in this new study the authors used new technical approaches to establish the validity of the theory.

Philipp Khaitovich, from the Max-Planck-Institute, led a collaboration of researchers from Cambridge, Leipzig and Shanghai who investigated brains from healthy and schizophrenic humans and compared them with chimpanzee and rhesus macaque brains.

They then looked for differences in gene expression and metabolite concentrations and, as Khaitovich explained; "identified molecular mechanisms involved in the evolution of human cognitive abilities by combining biological data from two research directions: evolutionary and medical."

They identified the molecular changes that took place over the course of human evolution and also considered the molecular changes observed in schizophrenia. They found that expression levels of many genes and metabolites that are altered in schizophrenia, especially those related to energy metabolism, also changed rapidly during evolution. "Our new research suggests that schizophrenia is a by-product of the increased metabolic demands brought about during human brain evolution," said Khaitovich.

"Our brains are unique among all species in their enormous metabolic demand. If we can explain how our brains sustain such a tremendous metabolic flow, we will have a much better chance to understand how the brain works and why it sometimes breaks," concluded Khaitovich.

The Full Paper
Boffins Investigate Schizophrenia Genes
Sexual Success And The Schizoid Factor
Microorganisms Behind Schizophrenia And Alzheimer's?

Source: Genome Biology