Mixing senses: synaesthesia taught to adults

Brain training for synaesthesia — where you mix up sensory information — may be just around the corner. People have been taught to experience a form of synaesthesia where letters     1     as certain colours, in their everyday life.

By the end of the nine-week course, most of the volunteers were seeing text in the real world take on particular colours, on road signs, for example. “The colour     2     pops into my head as soon as I saw the words on the road sign,” said one participant.

Synaesthesia is thought to result from people’s brains developing in such a way that their sensory     3     get mixed up. So “Tuesday” might evoke (导致) the colour pink, for example, or the word “tree” might taste like popcorn. Early life experiences may play a role — some synaesthetes report that their letter-colour     4     match the colours of a childhood alphabet or fridge magnets. But is it something you can learn as an adult?

Two years ago researchers made some aspects of the condition by getting people to read books where some of the letters were printed in certain colours. This improved their scores on tests but didn’t     5     out of the lab.

What if people     6     more intense training? Daniel Bor at the University of Sussex, UK, gave people daily half-hour training courses to teach them 13 letter-colour associations, using     7     harder tasks. The volunteers also practised with specially coloured e-books. As well as passing the lab tests, 9 of the 14 volunteers reported seeing coloured letters to varying extents when they read     8     black text. Many saw effects by week five, and some had synaesthetic experiences daily. Their power     9     once the training stopped.

The training had a(n)     10     benefit too. The volunteers gained 12 points in IQ tests by the end of training. However, this may be a general benefit of intensive training with memory-related tasks, says Bor, who adds that he may in future put the training tools online.

A failed study, a happy accident and a promising treatment for blindness In the textbooks, science is simple. You come up with an idea, put it to the test, and then accept it or reject it depending on what your experiments reveal. In the real world, though, things are rarely that straightforward, as a paper just published in Science Translational Medicine shows.

The disease in question is Leber hereditary optic neuropathy (LHON). A defective gene in a patient’s mitochondria — the tiny structures that provide a cell’s energy — causes retinal cells to die. That leads to sudden and rapid loss of sight, with many     1     becoming legally blind within a year. It affects between one in 30,000 and one in 50,000 people. Men in their 20s and 30s are particularly susceptible. Treatment is limited and not quite effective.

Since most cases are caused by a mutation (突变) in a single gene, LHON is a good     2     for gene therapy, a form of genetic engineering which aims to replace the defective gene with a working one. With that in mind, Dr Yu-Wai-Man, an ophthalmologist at Cambridge University, and his colleagues loaded up a (an)     3     virus with a corrected copy of the gene and injected it into their patients’ eyes.

Many viruses can insert their genes into the DNA of their hosts. That is     4     a bad thing, because cells so subverted (破坏) produce more copies of the virus. In this case, the hope was that infection would be a good thing. The defanged virus could not     5    . But it was capable of replacing the damaged gene with a working copy.

Most medical studies make use of a control group, against which the     6     of the treatment can be measured. Here, the researchers controlled the experiment by injecting only one of each patient’s eyes - chosen at random - with the virus. The other eye was given a sham injection, in which a syringe (注射器) was     7     against the eyes, but nothing came out of it. Using two eyes in the same patient makes for a perfect control: their genetic make-up is     8    , and any confusing lifestyle factors are removed from the equation.

The researchers had hoped to see a big improvement in the treated eyes, compared with the untreated ones. They did not, and for that reason the study failed in its primary objective. Instead, in more than three-quarters of their patients, they saw substantial     9     in both eyes.

On the face of it, that was bizarre. Only one eye had received the treatment, after all. The virus, it seems, had found a way to travel from one eye to the other, probably via the optic nerve. Although it had a happy outcome in this case, the prospect of a gene-therapy virus travelling to places it is not intended to go might worry regulators.

And, though the study was     10     a failure, its practical success means that an effective treatment for LHON may at last be in reach. GenSight Biologics, the company that has developed the treatment, has already sent its results to Europe’s medical regulator. It hopes to hear back by the end of 2021.