It's always confusing. When we talk about seasonal flu, we kind of lump them together because it happens so frequently. If you go back into a person's lifetime and see that they developed early-onset dementia or Parkinson's, they may have had several episodes of flu, so you don't definitively know. The difference with what happened in 1918 or 1957 or 1964 was that those were more large antigenic shifts, so our immune systems don't recognize them as well. There's a greater chance that we have a higher level of inflammatory responses with the infection and that respiratory infection with inflammatory responses often trigger neuroinflammation responses that can lead to this type of progression.
What I was referring to is that we've been studying—and I'm new to the neurosciences field to a certain extent, and I've gotten a rude lesson, if you will—neurodegenerative diseases for 30 years, and in that period of time we've never developed a treatment that dealt with early-onset aspects of diseases. Now we have something that occurs a little bit earlier, that is not approved in this country, but when you look at it, our drug development pipeline for Alzheimer's and Parkinson's is very, very poor as compared to that for other diseases, and that's because we can't define when the triggers have occurred.
We know what's happened in the past and know what potentially happens now and even the signs and symptoms that we're discussing today in the near term for long-term COVID, which are already causing pretty significant cognitive impairments and which are possibly also associated with the advancement of even cardiovascular diseases, clots, etc. What we're looking at is the ability to define the disease and the triggers and then to make some inroads in treatment, especially now that, again—and this is hard to share—we have these amazing animal models in which we can induce the same diseases. We then apply touchscreen cognitive tests in those animals the same way we do in humans, with the same types of tests, and then look at the treatments that might be available already—and how they might impact mouse studies, for example—and then apply them to humans, especially with approved drugs. These are types of things we can never study unless we know the trigger and, of course, establish what those biomarkers are.
One of the things I fear is that a lot of biomarkers can be very hard to assess, as Dr. Falcone indicated, and the other thing Ms. Goulding indicated as well was the availability of those diagnostic and disease-monitoring tools. I think we'll have to be relying on neurological imaging quite a bit in diagnosis, disease progression and the effects of treatment.