In 2006, however, Schurmans was flabbergasted when he came across a Swedish study: 'biopsies carried out on patients affected by Alzheimer's Disease during this study showed the presence of a particularly high quantity of ITPKB messenger RNA in the sampled tissues'. Once he got over the shock, Schurmans was determined to find out more about the role of ITPKB in Alzheimer's Disease. He contacted Professor Jean-Pierre Brion at the Université Libre de Bruxelles, who specialised in Alzheimer's Disease. 'The idea was to combine our respective expertise, his in the area of this disease and mine in the area of the role of ITPKB and knock-out mice', explains Stéphane Schurmans.

Senile plaques and the ITPKB enzyme, a relationship of cause and effect?

Together, the two teams therefore decided to research the role of ITPKB in Alzheimer's Disease. 'The Swedish study showed a high level of ITPKB mRNA in patients but we wanted to check whether this coincided with a higher quantity of ITPKB protein in the cortex', explains Professor Schurmans. Samples obtained by Professor Jean-Pierre Brion enabled researchers to investigate this further, concluding that abnormally high quantities of the ITPKB protein were also present in the cortices of patients suffering from Alzheimer's Disease. In light of these very positive results, the scientists continued their work to identify where this protein is expressed. 'Sections taken from the brains of deceased patients who had Alzheimer's Disease show that ITPKB is largely localised in the neurons surrounding the amyloid plaques', reveals Schurmans. One of the characteristic signs of Alzheimer's Disease is the formation of amyloid plaques, also known as senile plaques. 'These are extracellular aggregates formed from amyloid peptides which precipitate and form plaques between the neurons. This is one of the causes of the disease', continues the Professor. Indeed, these senile plaques prevent the communication of information from one neuron to another. It should be noted that the neurons around the senile plaques are strongly suspected of secreting amyloid peptides' he adds.