How A Gene Mutation That Leads To Blindness Might Also Increase Intelligence

Fruit flies share the RIMS1 gene with us, allowing an investigation of how a mutation in the gene may cause higher intelligence through stronger signaling between neurons. Image credit: Swen Reichhold/Leipzig University

It's a common enough getting to know you question: would you trade a physical attribute such as beauty for extra IQ points? What has always seemed entirely hypothetical could be very real if an astounding claim turns out to be true. In this case, what would be given up is not good looks, but the capacity to see. The gene variation in question causes a rare form of blindness.

The CORD7 (cone-rod dystrophy 7) mutation of the RIMS1 gene is just one of many rare alterations to the human genetic code that can take away our sight. However, researchers at the Universities of Würzburg and Leipzig were struck by reports that people with the condition score unusually well on tests of verbal IQ.

A team led by Professors Tobias Langenhan and Manfred Heckmann report in Brain that the mutation alters the way brain cells communicate with each other, providing a biological basis for the reports.

The adaptability of the brain has been a major area of research in recent years, most famously in the way people who lose one sense develop compensatory strengths in others. However, according to a paper Langenhan and Heckmann read, there is more to this in the case of the CORD7 mutations. The loss of eyesight does not begin until middle age, yet people with the mutation display exceptional intelligence as children.

"It's very rare for a mutation to lead to improvement rather than loss of function," Langenhan said in a statement. Moreover, while we know of some gene variations that provide advantages to aspects of the body such as the digestive and immune systems, nothing equivalent has been found for the brain, despite false claims promoted by racial realists white supremacists

Consequently, if what has been said about CORD7 is true, it's a first, making this a strong case of “extraordinary claims need extraordinary proof.” It's hard to get that proof by studying humans alone, however. You won't get ethics approvals to do a random controlled trial that would involve blinding people even if the genetic engineering technology and consent were both available.

However, CORD7 affects the synapses that pass messages between neurons and Langenhan and Heckmann have been studying synapses in fruit flies for years. On investigation, they found the gene that CORD7 affects has a counterpart in flies. CRISPR technology gave the pair the opportunity to induce the mutation in the flies and observe the results.

Tests of fruit flies' verbal intelligence would be, well, fruitless, but Langenhan said, “it was our assumption that the mutation makes patients so clever because it improves communication between the neurons which involve the injured protein." If so, the pair reasoned, the effects should be detectable in the insects' far more simple brains.

"We actually observed that the animals with the mutation showed a much increased transmission of information at the synapses,” Langenhan said. “This amazing effect on the fly synapses is probably found in the same or a similar way in human patients, and could explain their increased cognitive performance, but also their blindness.”

The mutation appears to cause components of the transmitting nerve cell to bunch up and release more neurotransmitters. It's the molecular equivalent of the person at a party who gets in closer and shouts loudly – great for getting the message across over interfering noise, but there's a price to pay. In this case, that price comes in damage to receptor cells in the retina.

If the work is correct, it leads to some rather crucial questions: could CORD7 mutation be modified so that we can boost humans' intelligence while maintaining our sight? If it can, would it be ethical to do it? It will probably be a long time before we have an answer to the first, but we might need it to ponder the second.

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