A research team from the Yerkes National Primate
Research Center, the Salk Institute and the University of California–
Los Angeles (UCLA) has identified genes in the cerebral cortex that
differ in levels of activity between humans and nonhuman primates,
including chimpanzees and rhesus monkeys.
These findings, which appear in the online journal of the Proceedings
of the National Academy of Sciences, may provide essential
clues to the unusual cognitive abilities of humans. They also may
help researchers understand why humans have a longer lifespan than
other primates and yet are so vulnerable to age-related, neurodegenerative
Because the DNA sequences of humans are similar to those of chimpanzees,
scientists long have speculated that differences in the activity
levels of particular genes, otherwise known as gene expression—and,
as a result, the amounts of particular proteins cells produce—are
what distinguish humans from chimpanzees. The recent sequencing
of the human genome has led to the development of "gene chips"
that enable researchers to examine the expression levels of thousands
of genes at a time, as well as compare expression levels in different
Using gene chips to compare samples of the cerebral cortex of humans,
chimpanzees and rhesus monkeys, the three-pronged research team
identified 91 genes that are expressed in different amounts in humans
compared to the other primate species. Upon further study, the team
observed 83 of these genes showed higher levels of activity in humans,
and as a result, regulated neural activity.
"When we looked at other tissues, such as heart and liver,
we found nearly equal numbers of genes showing higher or lower levels
of expression in humans as compared to chimpanzees and rhesus,"
said Todd Preuss, associate research professor of neuroscience at
Yerkes. "The changes in gene activity in the cortex suggest
increases in the rate of brain activity, providing a basis for the
evolution of the enhanced cognitive abilities in humans."
The researchers also found the human brain shows increased expression
of genes that protect against activity-related damage. This finding
may help explain why humans have the potential to live decades longer
than other primates, but also why humans are especially vulnerable
to age-related, neurodegenerative diseases such as Alzheimer’s.
"It is probable that the combination of long lifespan and high
neural activity makes humans particularly vulnerable to neurodegenerative
disease," said Mario Caceres, Yerkes postdoctoral fellow and
lead investigator on the study. "Activity-related damage accumulates
with age and has the potential to cause catastrophic breakdown late
in life. By understanding how humans protect their brains from activity-related
damage, we hope to better understand why those mechanisms fail."