Like most scientific discoveries, it was developed out of the University of Brescia by a little bit of serendipity. The scientists there had been working at The Weizmann Institute in Israel for a number of years, came back to Italy, continued doing research into P53 and Alzheimer’s. And then they were looking for specific markers to try and predict early what was going on with Alzheimer’s...
Like most scientific discoveries, it was developed out of the University of Brescia by a little bit of serendipity. The scientists there had been working at The Weizmann Institute in Israel for a number of years, came back to Italy, continued doing research into P53 and Alzheimer’s. And then they were looking for specific markers to try and predict early what was going on with Alzheimer’s. And they were looking at blood, and plasma, and other such materials and mediums.
They identified that unfolded P53, or a unfolded variant, was present very early and that it was specific to Alzheimer’s compared to other markers that were present at the same time. And what we then determined with further research and investigation was that, basically this unfolded variant is unique to Alzheimer’s, and this unfolded variant is caused by the breakdown of the post translational modification of the P53.
And basically, it’s an unfolded variant of the P53, which enables us to target really a region that is not normally present with antibodies so we can bind to it. And that marker therefore tells us that the P53 breakdown is changing the pathway, is causing an increased probability of Alzheimer’s being caused.
And we’ve done two major studies. We used a 224 patient study from the AIBL cohort longitudinal. That gave us our original discovery cohort and the performance targets that we were looking at, which were very high. Over 90% for a PPV and NPV.
Then we took a completely new cohort of over 482 patients, again longitudinal, with data from 10 years worth of patient studies, analyzed that, and we still got a PPV over 95% for the risk of decline within six years. And an NPV over 95% saying, “You will not decline into Alzheimer’s in that six-year period.”
Now, that data’s phenomenally powerful. We’re replicating that now. We’re doing that in ADRC and the ADNE cohort, and we hope to have published that before the end of the year, maybe next year, where we’ve got maybe another 600 or 700 patients from each cohort showing the same performance in different demographics.
So obviously, the data I just discussed is the prognostic performance and that gives us fantastic AUCs, which means that we can use those with patients, clinicians, and also in the clinical market to help pharmaceutical companies look at their buried treasures, their fallen angels, find new products and new targets, and basically accelerate the development of drugs, because we can enable you to identify the progressors, so that you’ll know for your clinical trial, which patients are going to be used and who are going to decline.
But additionally, one of the byproducts of this test is that it classifies the stage of the disease, in terms of are you cognitive normal, are you MCI, or are you AD at the time of our treatment? Our test I should say. So basically, you get told you’re a progressor or not. If you are a progressor, the results of our test also gives you a binary readout, which says you’re either a cognitive normal, MCI, or AD patient, even if you’re symptomatic or asymptomatic.
So you don’t need a PET scan, you don’t need a CSF analysis. Basically, the readout from a prognostic point of view is accurate. Then additionally, you get a diagnostic of what stage you are at the time of testing, even though you may not be showing symptoms.
