Scientists identify schizophrenia's 'Rosetta Stone' gene

Scientists have identified a critical function of what they believe to be schizophrenia’s “Rosetta Stone” gene that could hold the key to decoding the function of all genes involved in the disease.

The breakthrough has revealed a vulnerable period in the early stages of the brain’s development that researchers hope can be targeted for future efforts in reversing schizophrenia.

In a paper published today in the journal Science, neuroscientists from Cardiff University describe having uncovered the previously unknown influence of a gene in ensuring healthy brain development.

The gene is known as ‘disrupted in schizophrenia-1’ (DISC-1). Past studies have shown that when mutated, the gene is a high risk factor for mental illness including schizophrenia, major clinical depression and bipolar disorder.

The aim of this latest study was to determine whether DISC-1’s interactions with other proteins, early on in the brain’s development, had a bearing on the brain’s ability to adapt its structure and function (also known as ‘plasticity’) later on in adulthood.

Many genes responsible for the creation of synaptic proteins have previously shown to be strongly linked to schizophrenia and other brain disorders, but until now the reasons have not been understood.

The team, led by Professor Kevin Fox from Cardiff University’s School of Biosciences, found that in order for healthy development of the brain’s synapses to take place, the DISC-1 gene first needs to bind with two other molecules known as ‘Lis’ and ‘Nudel’.

Their experiments in mice revealed that by preventing DISC-1 from binding with these molecules - using a protein-releasing drug called Tamoxifen at an early stage of the brain’s development - it would lack plasticity once it grows to its adult state, preventing cells (cortical neurons) in the brain’s largest region from being able to form synapses.

The ability to form coherent thoughts and to properly perceive the world is damaged as a consequence of this.

Preventing DISC-1 from binding with ‘Lis’ and ‘Nudel’ molecules, when the brain was fully formed, showed no effect on its plasticity. However, the researchers were able to pinpoint a seven-day window early on in the brain’s development - one week after birth - where failure to bind had an irreversible effect on the brain’s plasticity later on in life.


wonder if this will lead to anything in the near future, sounds like good news.

I’ve read so many “we’ve found the grail gene” stories in the past 15 years than I have to confess I no longer taken any new one seriously. I always hope someone is “right,” but it never seems to turn out that way.


Some, e.g. Minkowski observed, that schizophrenia is more of a disorder of the integration of mental functions rather than an impairment in any specific mental function (though some may be impaired). If a gene responsible for plasticity is indeed the key to it, what is interesting to me is how plasticity is related to the integration of mental functions. Here, the notion seems to be employed as the capacity to form new synapses. As such it seems to me to be a rather coarse-grained concept to account for the disintegration of mental functions, while each of these functions individually need not decline, though may do so. I am only saying so under the impression that specific mental functions will (need to) form new synapses in their execution as well - and I may be confused here.

The Daily Mail (not my favourite newspaper) talks of screening and treating infants to prevent the condition developing.

So as Professor Fox is the one discovering this maybe we could be called people with Fox Syndrome - I’d rather be Foxy than Schizophrenic which is Greek for SPLIT MIND and so doesn’t mean much other than re-enforcing the notion of split personality - Jeckyl and Hyde.

I remember in 1996 I went with my elder sister to the Schizophrenia Association of Great Britain headquarters in Bangor Wales. They were collecting DNA/blood samples of people with schizophrenia and their immediate family members. They were trying to find the gene. I do hope that Professor Fox does make a breakthrough and find THE CAUSE.

In 50 years they haven’t changed the way antipsychotics work on the brain, I don’t think they’ll find answers that soon. They are always “discovering” and “discovering” “new” things but the things remain basically the same.

Originally the first neuroleptics were antihistamines and were discovered to treat psychosis. I’d love for a cure to be found for future generations - live in hope.

Most of the time they seem intent on slightly altering a previous med (abilify-rexulti for example) to ensure profits are maintained than doing anything innovative . Psychiatric drug research has been in the doldrums for years.

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In the UK Schizophrenia used to be known as a “Cinderella” illness in that hardly any money was spent on research. I can remember the older style medications and they were not a good experience. I was put on Stellazine, Orap, and then Modecate injections and it wasn’t pleasant. I hope that even if the cause is never identified, that they can get nearer and nearer to finding better and better medications.

And I was given Largactyl - who could forget that one!

Back in the 70s/80s at various points I was on largactyl, mellaril,veractil,stelazine, orap coupled with redeptin injections and before the redeptin possibly modecate(hard to remember).

Was there one called DIPIXYL - an injection - I had that for a while as well. Modecate 9 years on that - the night terrors it gave me were TERRIBLE - switched to Olanzapine and have never had the night terrors since.

Yes- depixol. I remember the old injections used to hurt in the way the current ones don’t. I think there was a tendency to give higher doses back then hence being on an oral med and an injection. Nowadays it’s usually one or the other. Liquid largactyl or mellaril was rather disgusting.

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They “improve” - as they should - some of the side effects but the problem remains. All I hear in the hospital is, the meds keep getting better and better. I can’t stand that argument.

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The old injections used to be in an oil suspension so they had to use thicker needles for it - sometimes they REALLY stung. My GP had the knack and could do it with a thinner needle, but if the nurse did it she used the thicker ones - really long thicker ones lol!

I was on Clopixol depot for some time. They also had to use the thicker needles. I don’t like that oil based injections as they never seem to release well in the muscle. Later on they had to inject the stuff in the muscle of my upper leg

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They used to do mine high on the backside, into the muscle. If it hit a nerve I used to jump lol!

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