A recent study conducted by researchers at the University of California has found a gene which they believe is responsible for IQ differences up to around 6 points, according for 3 percent of intelligence differences among humans. A specific version of the KL gene, known as KL-VS, has been shown to promote longevity, but what 3 independent studies have also suggested is that it plays an important role in mediating intelligence differences among the human population. Intelligence tests were administered to 220 volunteers, aged 52-85, and researchers found that those with a VS version of the gene exhibited higher intelligence scores than those without the variant.
The other two independent studies, as noted, found similar results, meaning that the effect of this gene variant’s effects have been measured in 718 people, a fifth of whom possessed the KL-VS variant. What makes the study unique is that, although previous genes, such as HMGA2 and NPTN, were shown to correlate with general intelligence, the correlation was not nearly as high as it appears to be ewith the KL-VS gene.
In order to determine whether or not the correlation belied real causation, the researchers decided to test the effect of KL-VS on mice. The “murine equivalent” of KL-VS genes were added to mice genes, causing an increase in their klotho levels; an effect which is also observed in humans who test positive for the KL-VS variant. The researchers found that the mice performed better at navigating mazes, and also exhibited better memories, than ordinary control mice. In addition to their superior intelligence performance levels, the mice also exhibited neurobiological abnormalities providing evidence that they were indeed more intelligence.
The brains of these mice exhibited synaptic abormalities relative to other mice. The NMDA receptors in the hippocampi and frontal cortices, both of which are important brain structures involved in the formation of memory, of the genetically modified mice doubled the number of a molecular subunit known as GluN2B; GLuN2B having been previously found to be related in important respects to cognitive performance. A writer from economist.com explains thus:
Signals cross synapses in chemical form. The most common messenger chemical, known as glutamate, is picked up by the receiving cell using molecules called NMDA receptors. It is known from previous work that glutamate stimulation of NMDA, or the lack of it, can strengthen or weaken synaptic connections. This is believed to be the basis of memory.
The team’s genetic engineering changed the nature of the NMDA receptors in the mice’s hippocampuses and frontal cortices—two regions of the brain particularly involved in memory formation—by doubling in them the number of a particular sort of molecular subunit, GluN2B. Previous research has found links between GluN2B levels and cognitive performance. Dr Dubal and Dr Mucke discovered that blocking GluN2B with a drug called ifenprodil abolished the genetically engineered mice’s advantage. That suggests klotho works its magic, at least in part, by increasing the number of GluN2B subunits in the NMDA receptors of the brain’s memory and learning circuits.