Scientists have identified a mutation that they say could help
explain why human cognitive abilities are so different from those of
other animals.
Past searches for such genetic changes have had spotty success. A study
last year did find mutations unique to humans in a gene called HAR1F,
tied to brain development and possibly brain size. But it didn't
clarify for certain whether the gene also enhances mental
capacities. Another gene, called FOXP2, has been linked to language
abilities.
The new study found that human brains have a unique form of a molecule
implicated in learning and memory, called neuropsin.
This new form would have originated less than five million years
ago-later than when the human lineage split off in evolution from its
closest ancestors, chimps, some six million years ago. Humans and chimp
genomes vary by an estimated 1.2 percent.
The study is to appear in an upcoming online issue of the research
journal Human Mutation.
Bing Su of the Chinese Academy of Sciences in Kunming, China and
colleagues analyzed humans and several species of apes and monkeys.
They found that humans alone had a particularly long form of the neuropsin
molecule called type II neuropsin. Although the precise function of
neuropsin, a protein, remains unclear, it has been found in mice to help
control a process that underlies learning and memory formation. In
this process, called long-term potentiation, new information prompts
brain cells to gradually change their tendencies to pass along signals
to other cells.
The change in the protein, Su and colleagues said, was in turn due to a
change in a so-called splicing site of the gene that codes for its
production. This in essence means the gene's code is edited
differently as it's used to create a finished molecule. The findings
"underscore the potential importance of the creation of novel
splicing forms in the central nervous system in the emergence of human
cognition," the researchers wrote. They added that future research
will have to clarify further what type II neuropsin does.
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