On a hot May day in 1967 Celtic earned their place in the history books by beating Internazionale Milan in the final of the European Cup. Celtic were the first British football team to claim that trophy. Their hero was a slightly built, red-haired man with a special ability to take the ball past the defender. Jimmy Johnstone will always be known as “Jinky” because he was so nimble on his feet.

Sadly, in recent months, Jinky has lost this exceptional agility. He is afflicted by motor neuron disease. MND is no respecter of ability. It is the name given to a group of related diseases affecting the nerve cells which activate the body’s muscles. Degeneration of these motor neurons leads to weakness and wasting of muscles. This may start in one arm or leg, but the “creeping paralysis” always becomes more generalised, rendering the simplest actions impossible. When the disease affects muscles in the tongue and throat, speaking and swallowing become increasingly difficult. Ultimately sufferers die because they can no longer breathe.

The disease claims the lives of 1,200 people a year in the UK. The average age at onset is about 55 and survival is only three years from the first symptoms. Despite decades of research, the disease is not well understood and there is no effective treatment. Given that a single drug trial in MND patients costs as much as £20 million and takes two years to complete, a cure seems a distant hope. Our team of scientists aim to bring that cure closer to our reach. Ideally, we would like to directly observe the motor neurons of people affected by the disease as they degenerate, but they are in the brain and spinal cord — areas inaccessible to research. So what can we do? We can reproduce diseased motor neurones in the laboratory using nuclear transfer technology (cloning) to create cells that have an MND-causing gene defect. These can provide us with an endless supply of motor nerve cells that are almost identical to those of the patient. Then we can study the disease process in minute detail and, more importantly, screen hundreds of thousands of compounds that might potentially arrest or even reverse the degeneration.

In about 10 per cent of cases, MND runs in families, and is due to an inherited gene defect: we call these familial cases.There is no family history in the remaining cases, but they may still reflect a genetic susceptibility. After 20 years of research one gene has been discovered, called SOD1, and mutations in this particular gene can be found in 20 per cent of inherited cases and some of the other “sporadic” cases of MND. The genes responsible for MND in the remaining sporadic cases are unknown and have proved difficult to locate and identify using traditional gene-hunting strategies. Cloning will allow us to study the effects of these gene defects on motor neurons without having to track them down. There is no other way to achieve this aim.

There are many different types of cloning. Our research will involve therapeutic cloning: the process of generating human embryonic stem cells that are genetically identical to the patients’ cells. This is not reproductive cloning: the eggs will not be allowed to grow beyond 14 days and once the stem cells have been removed, the remaining cells will be destroyed. Even so, legislation to permit such research was passed in the UK only in 2002 and ours is the second licence to be granted to date. All aspects of the research require ethical approval from local committees and a licence from the Human Fertilisation and Embryology Authority. Dolly the sheep, created at the Roslin Institute in 1996 and the first mammal to be successfully cloned from an adult cell, was part of an altogether different project: reproductive cloning, for agricultural research. There is a continued ban on human reproductive cloning — the creation of new human beings.

Entirely new opportunities to study many genetic diseases will become available through therapeutic cloning. But how exactly does it work? Embryonic stem cells are special cells that can be derived from early embryos. They have the ability to form all of the different cells that make up complex tissues in the adult human body. Scientists are now working out which chemical signals are required to induce stem cells to become almost any cell type. The cloning process will involve the transfer of genetic information from a cell of a familial MND patient into an unfertilised egg from which the genetic information has been removed. All the cells in the developing embryo and their stem cells will contain the genetic blueprint of the original patient, including the MND-causing gene defect. We now know how to turn these embryonic stem cells into motor neurons that can be grown in cell culture so that the effects of the defective gene can be studied in the laboratory.

This process could make a unique contribution to studies of any inherited disease in which the gene that is responsible has not been identified. If the genetic defect has been identified, an alternative approach is available: the defective gene can be deliberately introduced into healthy embryonic stem cells and then the appropriate chemical signals are introduced, in order to derive mature cells that are relevant to that particular disease. In our project it will be particularly informative to compare motor neurons with several different mutations. SOD1 mutations will be introduced into existing stem cells while cloned embryos will provide cells with different, unknown mutations.

Cloning is the only effective way to study MND. It is never possible to predict the outcome of research, nor can we estimate the time required. Nevertheless, the project holds out the possibility that one day we will discover the first effective treatments for this terrible disease.