Discover The Power Of Blood Tests

Hans Frykman, MD, PhD

Thanks, Heather, for the invitation. It’s my pleasure to be here.

Dale Bredesen, MD

Let’s talk initially about why these tests are so good. We know why this is turning out to be such a good test. neurocode, as I understand currently, is offering p-Tau 217. But also, you are running neural filament light and GFAP, Glial Fibrillary Acidic Protein. Is that correct?

Hans Frykman, MD, PhD

This is correct, yes. We also offer spinal tests. The big change in 2024 is that we now have these blood tests, as you mentioned, and the blood tests are revolutionary because we have gone from the first such test that was at all interesting in 2017 out of a group in Japan to now having something clinically useful. The last time this happened in clinical chemistry on a blood test was when we got troponin for heart attacks. Which was quite a few years ago. It’s a very big thing happening in the clinical chemistry world.

Dale Bredesen, MD

It’s a great point. when I was training way back in the 1970s, and we would be getting a CPK-MB to see if someone had had a myocardial infarction. We’ve come a long way with troponin since then. It’s hard to overstate how important it is because we’re always trying to convince people. Please don’t wait. We can reverse cognitive decline. We can prevent cognitive decline. But it is progressively more and more difficult as you wait. Neurologists and other physicians have said for years, there’s not a lot we can do; just wait. It’s probably going to be okay. Then, of course, people march right through MCI, etc. We know from serial PET scans and spinal taps that you do have changes about 20 years before a diagnosis. That’s pretty typical. You can see it coming.

There is a lot you can do about it, but people don’t want to do this because, for one thing, they don’t want spinal taps, and for another thing, they don’t want to know. Now everything has flipped around. We wanted to check earlier. We want to find out. Just to give a recent example, there is one person out there who will remain anonymous. Who did happen to get this evaluated did happen to find that although this person was at risk and had minimal symptoms, it was a forty-four-four. He had a very high p-tau and had just begun to do some of the appropriate things from a multi-modal protocol. Sure enough, the p-tau is coming down. That we will be using this. 

As part of the ongoing trial that we have at six sites, we are working with the neurocode to do these very tests. We will be following the patients. Where do they start with their p-tau? Where do they end up? Let’s start by talking about the comparison here. If you look at the two common ones, which are the Abeta 42/40 ratio and p-tau. And p-tau, there was a p-tau 181. But it’s turning out that p-tau217 is superior to p-tau181: Let’s go back to the Abeta 42/40 ratio. When you begin to have changes associated with your brain signaling that are going to ultimately lead to Alzheimer’s, how much of a change do you see in the 42 to 40 ratio? How robust of a test is this?

Hans Frykman, MD, PhD

So Abeta 42/40 ratio is an excellent test to detect early pathology because that’s what you detect. It’s always important to say that the tests that we do are detecting pathology rather than a disease because it can lead to a disease and it’s associated with the disease, but it’s not. It’s biomarkers that lead to pathology. that’s an important distinction. Abeta 42/40 ratio as a service is an excellent test for spinal fluid. The reason for that is that there’s liquid inside the spinal system, and surrounding the brain’s CSF is protected from the outside. In that system, the Abeta 42 gets used up. We measure a lowering of Abeta 42, and then we normalize the Abeta 40, which is a much more abundant protein. By doing that, we get a very robust signal for MCI and for mild and even moderate to severe Alzheimer’s.But the most important thing is that we can detect MCI; we can detect mild Alzheimer’s with the CSF test and the spinal fluid test, and that has been FDA-approved for about a year and a half or two years. It’s been FDA-approved on two different platforms. It’s a test that’s unfortunately not covered either by the U.S. government or Medicare. But we do not use private insurance very much. However, it’s a very good test, but you have to get that spinal tap, and that is something that is not comfortable that you have to go in for the procedure or that the procedure is covered by insurance. But you have to go in for the procedure. You risk getting a headache or having many other side effects. As you said, it’s not something you want to do every year.

Dale Bredesen, MD

I did many of them as a neurologist, so they’re not fun to have. As pointed out, people can get spinal headaches, which can last for months. If you can get a blood test instead of a spinal fluid test, that’s a huge advantage.

Hans Frykman, MD, PhD

Now they’re in that CSF test. You can also measure p-tau181 and total tau, and the p-tau181 increases the validity of the signal of the Abeta 42/40 ratio. that makes that test more accurate. If you also add total tau, that can help you or can help a neurologist at least to differentiate Alzheimer’s versus other pathologies, especially tau pathologies, depending on where they are. It’s not Alzheimer’s that’s present, but there are other diseases present in other situations. We have four biomarkers, which, by the way, we are the only lab that provides all four in North America. We provide five because we also have a Neurofilament light, and the spinal fluid and data happen to be the earliest of all the biomarkers, and spinal fluid even before it Abeta 42/40, you will have a rise of NFL, Neurofilament light.

Dale Bredesen, MD

Let’s focus on the blood test for a moment here. You pointed out that these are excellent tests for the spinal fluid. But when you’re getting a blood test, what are you getting if you’re getting Abeta 42/40 blood tests?

Hans Frykman, MD, PhD

Excellent. If you tried to do that in blood, the Abeta 42/40 ratio that the test uses does not work in blood. The reason is that you have Abeta 42 which is decreasing in the brain when you go into these pathologies. If you’re going to measure something that is decreasing, that is, you get about a 40% decrease in spinal fluid but in blood, the problem is that the body outside the brain produces Abeta 42. The blood test is very complicated to measure. It’s not possible to measure. You have only an eight to 10% change.

Dale Bredesen, MD

Eight to 10% is all you change when you have that pathology.

Hans Frykman, MD, PhD

Exactly. I’m sorry to say, but there is this test, and for that reason, it’s not suitable to perform. There are labs; I’m not going to mention any names, but there are a couple of famous labs that perform that and even sell it directly to the public. This is very unfortunate because this test is useless. There’s no way to say it, but it’s useless. Let’s not discuss it. Let’s go further.

Dale Bredesen, MD

Why have you chosen the ones you’ve chosen? because they’re the best tests. To me, what’s exciting about the triad of p-tau217 Neurofilament Light and GFAP is that they give you three complementary pieces of information, all of which are very helpful. Let’s start with p-tau217, which shows multiple papers showing that it is highly predictive of the pathology of Alzheimer’s disease. But maybe the most important thing is: how early do you see that change? If we think of the presymptomatic phase, SCI, MCI, and dementia, where do you start seeing the p-tau217 increase?

Hans Frykman, MD, PhD

That’s a very good question. We don’t exactly know that in detail. There was a Daily Mail publication just a few days ago where it said, our test, which they were writing about as we were in Time Magazine, CNN, and Fox. Whether you are on the Atlantic or the Pacific Ocean, you were hearing about our test just last week. This test is probably not going to detect it 15 years ahead.  There’s no scientific proof of that. But you could have indications even years before you have symptoms; exactly how many years that it is, we don’t know at this time, but what we can say is that it’s probably going to be good enough to detect MCI in many cases, and it is certainly good enough to rule out MCI due to Alzheimer’s pathology, which is also important because lots of people are worried that they have MCI. They start forgetting, especially now after the pandemic. I had COVID several times, and I experienced some light memory loss after that. Many people have, honestly, different degrees of this. and, hopefully, that reverses in most people, and it likely will.

The feeling of not memorizing as you used to is terrifying and very sad and we can do a lot about it. If it’s Alzheimer’s disease, it’s better to detect it early. This is the best blood-based test there is available for that. I said we can rule out MCI; we can probably rule in MCI, meaning if you do have that, we can detect mild Alzheimer’s, which is still a stage that can be reversed. We want to change the sad fact that 79% of all Americans who get diagnosed with Alzheimer’s are diagnosed at the moderate-to-severe stage today, 79%. We are working with one of the big champions of this, a professor at Wake Forest who was previously at Mayo Clinic. Her name is Michelle Malkin. She’s a very dynamic young star in this field. She is pushing for this to be used at the primary care level. So we are entering into a very large clinical trial with her doing this at the primary care level. We are using the p-tau217 as a screening tool for MCI and mild Alzheimer’s just to get people diagnosed much earlier. This is funded by NIH, and we’re very excited to be part of that.

Dale Bredesen, MD

Let’s back up for one moment and just talk a little bit about tau itself. We think of tau as something that’s almost like bolts on the microtubules. It is something that stabilizes microtubules. At least from the biological side, it always made sense that if you are going to collapse your microtubules, if you are sending synaptic plastic signals and pulling back, you are going to phosphorylate your tail, which pops it off the microtubules, and now you can collapse. It’s a physiological process, but it also has implications for Alzheimer’s disease. How many amino acids are in tau?

Hans Frykman, MD, PhD

431 

Dale Bredesen, MD

How many phosphorylation sites?

Hans Frykman, MD, PhD

All those are many.

Dale Bredesen, MD

Many phosphorylation sites.

Hans Frykman, MD, PhD

I don’t know the exact number.

Dale Bredesen, MD

217 has turned out to be fairly specific for Alzheimer’s. I guess that’s the next point here, which is that when you see that increase in 217, it doesn’t appear to be due to vascular damage. It doesn’t appear to be due to other pathologies. What does it mean? How specific is that for Alzheimer’s-related pathology?

Hans Frykman, MD, PhD

That’s a very good question. It’s 95% specific. It’s 95% accurate. It’s a superb test. that is very equal to the spinal fluid tap.

Dale Bredesen, MD

Then the other point is, that we’ve been telling people for years that if you find out you are ApoE4 positive, please don’t worry. There’s a tremendous amount you can do for prevention. There’s a wonderful website set up by Julie G. the apoe4.info. We’re in the same situation here. Please do not worry if you find out that your p-tau217 is high; there is a lot you can do about it. As Hans indicated, this will come up fairly early so that you can do something about it. This is going to change instead of waiting. 

Now though, all the things we’ve been looking at—HS-CRP, insulin resistance, so forth and so on, various pathogens and toxins—those tell you why you’re at risk and why you’re having problems. This tells you if you’re having me; this tells you that the signaling is going on. They’re extremely complex, and again, they will give us the ability for many more people to get early diagnosis and therefore prevent pain and reversal, which is why this is such a game changer. Okay, now this site is 217 out of the 431 that you mentioned for Tau.

Hans Frykman, MD, PhD

441, sorry.

Dale Bredesen, MD

441, okay. This is a serine or threonine, or which is this?

Hans Frykman, MD, PhD

Threonine, I think it is.

Dale Bredesen, MD

Threonine. Is this the major kinase that is phosphorylated? Is it GSK-3 beta, or are there other kinases as well?

Hans Frykman, MD, PhD

That’s a good question. But no, there might be multiple.

Dale Bredesen, MD

Have you seen, of course, GSK-3 beta, something that can be inhibited with lithium? Have you seen reductions with people just using lithium, or has anyone looked at that?

Hans Frykman, MD, PhD

That’s a good question. I don’t know the answer to that.

Dale Bredesen, MD

All right. Go ahead.

Hans Frykman, MD, PhD

That could be just, all right.

Dale Bredesen, MD

This is going to tell you, and I should mention, in terms of its robustness, as you’ve pointed out, talk a little bit about how much change you see because it’s got a huge dynamic range.

Hans Frykman, MD, PhD

That’s very comforting. One of the reasons that this test is so good is that the difference between healthy controls that are age-matched and healthy controls is that we did PET scans of these healthy controls. We know that there are healthy people because, otherwise, as you pointed out, we can’t know somebody who can look very healthy and still not be so. We know that, and so compared to healthy controls where the person wants to have the disease, particularly if they have both amyloid and tau pathology, the differences are four and a half times greater. At least Four and a half times. It’s very large. This phosphorylation of this site is not huge in Alzheimer’s, but it is enough to measure very sensitive instruments, but far from it. There’s no phosphorylation going on at all in healthy controls. Your values should be very low if you’re healthy than if you have an elevation. 

The more elevation you have, the more pathology you have going on on a group level, at least. What I’m saying here is that the people who had amyloid pathology would have maybe two and a half to three times the elevation, while the people who had both amyloid and tau pathology had more like four and a half to five times the elevation. It rises through the continuum of the disease. As you go, you have a personal value, and that value rises as you progress. then, and in the same way, if you’re able to reverse Alzheimer’s, you can see a decrease. We have seen that with your patients. We have seen that in clinical trials, even though I am not a huge fan but we have seen that in clinical trials with the mob, donanemab, and so forth. 

Dale Bredesen, MD

There is a good point.

Hans Frykman, MD, PhD

There are many uses for these tests, not only as an initial screen diagnostic tool but also as a follow-up test. It’s important to connect. I just want to connect to pathology because people wonder how I have amyloid pathology and you’re measuring tau. Why? Why is that? The reason there is that once they block amyloid plaque attached to a nerve end, the signal goes upstream to the nucleus of this nerve cell, and the tau tangles get phosphorylated, and they happen to cause phosphorylation on many sites, as you indicated. But 217 is the most important site.

Dale Bredesen, MD

Very interesting. The great news is that not only can you see it relatively early on, at least not only does it reflect whether you have this pathology, but you can also use it as a tool to follow over time. Now, it’s important to know. Let’s say we get to time zero and start treating people. Presumably, we don’t want to measure it next week. What’s the appropriate time to follow up to see if it’s going in the right direction, i.e., back down?

Hans Frykman, MD, PhD

That’s the question we don’t have answers for. But at least three months, and probably six months, depends on how much therapy you do. Some people are very ambitious to follow your protocols, and some people take it more relaxed. If you have somebody who is very ambitious and wants to see a reversal, three months could even be possible. But the six months are probably more realistic in most cases.

Dale Bredesen, MD

Then let’s for a minute talk about the other tests, because these are very complementary. One of them is telling you, Is this an Alzheimer-related process? How long has it been going on, etc.? The second one, neurofilament light, is telling you, Is there neuronal damage? If you have frontotemporal dementia (ALS, do you also see it with things like CTE? If so, essentially any neuronal damage, is that fair to say?

Hans Frykman, MD, PhD

That’s very fair. then something more sinister: if you have the NFL that you have, it rises slowly in your life, and for us, our man, we can relate to that with PSA, so PSA A.L.S., but the same if you continue to measure your NFL for your life and then suddenly it takes off, meaning that you have longitudinal measurements of your NFL then you will probably have the earliest biomarker it is presently available to detect something sinister is starting to happen in your brain. So, NFL, I encourage people to measure. If it’s normal, then fine. You probably don’t have to measure it more than every second year or so. Similar to what you would do if you were a male and a measuring PSA. And in the case of PSA, when it ticks off and bangs up, you go for the scans, and then you’re probably going for a biopsy, and so forth. In the same way here with the NFL, if you measure it longitudinally and it goes up, but if you don’t feel anything, you should still probably be concerned because it’s a very good biomarker. It’s very exact. The test that we have today is superb. It was developed quite several years ago by a group in Northern Sweden.  Everybody uses the same test, but you can use different platforms. In our case, we use it on a more professional platform, so we have moved it to the next level. I would say it’s the second third-generation test. Working with the Japanese group in this case, this was the first lab setting up this more robust NFL test. We are very happy with measuring the NFL. I don’t think it’s something that, let’s say, you have a high p-tau and your NFL is normal. There’s no reason for you to start re-measuring the NFL, when you should follow your p-tau to see that it normalizes.

Dale Bredesen, MD

That’s a good point. For people that you’ve looked at who do have Alzheimer’s disease and have high p-taus, how often do you see a normal NFL?

Hans Frykman, MD, PhD

Most of the time, So they are not that elevated, and in Alzheimer’s, they are mostly quite normal. However, if you do have a low or elevated NFL, then honestly, that means, just to be candid, that something more sinister is going on. and I’m talking about the NLS and all these things. There is a reason to measure nephrologists to check that that’s normal and that nothing else is going on. As there is sometimes overlap between different pathologies with Alzheimer’s, You want to check for that. It just gives you more information, and in most cases, it is probably a test. You don’t have to repeat that often. For the NFL, just one time, if you do have a traumatic brain injury, there is a reason to use the NFL. Also, it’s a very good test for traumatic brain injury, which is very predictive, and you can do it at a two-day serine when you have the injury and then at day seven.

Dale Bredesen, MD

One of the reasons I’m enthusiastic about it is that so many people will come in, and I’ve had some twitches; I’ve had some fasciculation. This is ALS, which is very hard to treat and typically terminal within three, three and a half years. Is that common, or is this just Benign fasciculation? If you have ALS, your NFL should be typically high, correct? 

Hans Frykman, MD, PhD

This is a good way to reassure people. It’s a rule-out test in this case. Yes, I agree. NFL is very good to use just to focus your attention on what’s going on. If it’s after the NFL is high, for example, and your treatment has to be a lot more aggressive, I don’t know exactly your protocol, but I imagine it to be quite different.

Dale Bredesen, MD

We don’t have a lot of data yet on LBD. The argument is that the approach we’ve used is tailored to the biochemistry of Alzheimer’s. We don’t know about this. We’ve had some good results with Lewy Body. We’ve had some good results with vascular dementia. We do not know about LBD yet.

Hans Frykman, MD, PhD

There’s a lot to do from there.

Dale Bredesen, MD

With Lewy Body Disease, since it’s turning out, there’s a lot of overlap between Lewy body and as John Q. Trojanowski, the pathology professor at UPenn, has shown most of the somewhere around 60% or so of Alzheimer’s autopsy cases have Abeta, Tau, TDP 43 and even have some synuclein in there. So there’s Lewy body pathology in many of these. I guess the first question is: if you have a pure Lewy body case, is the phosphoryl high, and is the NFL’s?

Hans Frykman, MD, PhD

No.

Dale Bredesen, MD

The p-tau will not be high in those cases. What about the NFL?

Hans Frykman, MD, PhD

The p-tau, no. The NFL? it’s a little bit elevated, but similar to Alzheimer’s. It’s not as much as it does have to do.

Dale Bredesen, MD

It’s a slower process, but what’s interesting is that the third test, GFAP, is again complimentary. This is looking at the astroglial response. Unfortunately, it’s not telling you the microglial response, but it’s telling you the astroglial response. As has been pointed out for years, that’s one of the early if you’re developing prion diseases like Creutzfeldt-Jakob disease or if you’re developing Alzheimer’s, one of the earliest changes is this astroglial response. Your GFAP is going to be not specific for Alzheimer’s but is going to be sensitive. When you’re looking at this, how commonly are you seeing increases in GFAP in Alzheimer’s cases?

Hans Frykman, MD, PhD

Now, that’s a lot of cases. It’s what’s proposed as the marker for Alzheimer’s by Charlotte Teunissen and our group in Amsterdam that says that the p-tau217 is much better now, but it still has great validity and value, particularly around inflammation. Yes, part of that. so you can think about Alzheimer’s as a small component, as you pointed out, and others. So this is the inflammation part.

Dale Bredesen, MD

When you get a look at it,  what’s the ongoing inflammatory component? Of course, again, you should be able to bring that down as you quell the inflammation and understand what’s driving it. I had a very interesting talk yesterday with Dr. Richard Horowitz, who is using Dapsone and getting very exciting results, including improvements in cognition with people. You look at these plaques in the brain, as Rudy Tanzi, of course, and Robert Moir pointed out years ago. Inside these things, there are pathogens. This amyloid is sequestered in an anti-microbial peptide. So if you can identify what’s inside those, then you have a leg up in terms of knocking down that pathology, which he’s doing very successfully with his Dapsone protocol.

Hans Frykman, MD, PhD

That’s very interesting. I didn’t hear about that. 

Dale Bredesen, MD

It’s an interesting drug because, of course, it has been used for years in leprosy. But as he’s pointing out, it is quite successful with Lyme disease and tick-borne illnesses, and he uses these pulse protocols that have been working very nicely. Of course, it has a nice anti-inflammatory effect. It’s got real potential for many people who have these pathogens. I don’t know that they have the pathogens. They just know that they have cognitive decline. Two more than that, and I guess let me ask before we move on: are these all plasma tests? Serum tests are whole.

Hans Frykman, MD, PhD

That’s critical. That’s correct. They’re all plasma tests. That is, if you take away the blood of the red blood cells, the white blood cells, and the plasma, The difference between serum and blood supply is not large compared to just one product. If there are plasma tests, it’s very standard to separate plasma from blood. and they’re very robust. All of these tests, particularly those p-tau217, last for four weeks outside the freezer or even in a refrigerator. Which is encouraging. so that’s built for a very good test. As I said, it’s funny because this is such a low, abundant protein that we wouldn’t have been able to measure these things ten years ago before these more sensitive instrumentation.

Dale Bredesen, MD

So then for p-tau, just in practical terms, it sounds like this can be shipped without ice. Is that right?

Hans Frykman, MD, PhD

We prefer it to be shipped with ice at least. In the summertime in the southern United States or other places, it gets hot. We don’t want to do that, but we prefer an ice pack at least. But an ice pack is going to be sufficient in this case.

Dale Bredesen, MD

What top tube, what color?

Hans Frykman, MD, PhD

It’s the purple top tube that you collect in, and then you transfer it to plasma. That was an EDTA tube, which had a purple top. then you take that spin it, and then transfer it so that most labs can do that. Most collection sites can do that. then you take it to plasma. 

Dale Bredesen, MD

I was just going to say that since you’ve been so important in developing these tests and so fundamentally involved with them, let me ask: as someone interested in understanding what’s going on in the brain of patients with neurodegeneration, I would love to see ultimately two other tests. You’re giving us something for neurons. You’ve given us something for Alzheimer’s. You’ve given us something for astrogliosis. How about macroglossia? What is the potential for seeing a microgliosis test? Then the other one would be mast cell activation. I love to know inside the brain: is there mast cell activation? What is the potential for developing those tests?

Hans Frykman, MD, PhD

There is that the field has particularly been dormant for so many years now. We can’t do this. We can’t do this. It was like before there was any before our Dr. Farber came to the Boston Children’s Hospital to start developing leukemia drugs. There was no hope for cancer  together with certain chemists at certain pharmaceutical companies, I should mention as well because there was not only Farber himself but, 

Dale Bredesen, MD

We saw that they just had to retract 37 papers that came out of Dana Farber a couple of days ago. I know that’s tough.

Hans Frykman, MD, PhD

What I want to say is that you set off in a whole avalanche. That’s what’s happening now, from not being possible to not being possible. We’re now getting confidence that we could do this for p-tau, which measures amyloid as well as tau pathology. If we can do that, we can do more, we already have the NFL, and we are, GFAP. We’re upgrading to an even better method this year for GFAP. There is something called a brain-derived tile, which is similar to tall towers, and the CSF measurements are coming later this year. The arsenal of tests will increase and will expand. At the same time, it’s important to educate people, particularly on how to read the results. We might have a separate discussion on just how to read the results, and maybe I can have some graphical explanations. If you see what you see in different situations, but that could be for a more interested group. This was a good talk, just explaining these tests for a more general, larger group.

Dale Bredesen, MD

I look forward to those. It’s going to be better, and it’s going to make fundamental changes in the field for people to know early on. When did they start measuring lipid changes, cholesterol changes when they were 19, what, six early sixties, or something like that? We’re entering the same point here where you can get an idea—a quite accurate idea—of what’s going on in your brain with these blood tests, which is just fabulous. Of course, it offers the chance to do something about it, especially early on. We’re going to see a whole wave of people who are trying to prevent people who have this in their families. As I’ve pointed out, this should be the last generation that worries about Alzheimer’s disease. Our daughters, my daughters, are now in their thirties. I would love for them not to worry about this. They should all get their p-tau checked when they turn 40, see where they stand, get it checked every few years, and find out if they’re doing well and if they’re not. There’s a lot you can do about it.

Hans Frykman, MD, PhD

I’m totally with you there, Dale. This is it; the work you’ve done is just amazing. When I grew up, we were immediately afraid of heart attacks and then of cancer. Now everybody is thinking about the brain. It’s with a certain actor in Hollywood getting FTD. This highlights the suffering that certain of these neurodegenerative diseases have. We are entering an era where people are going to be afraid of this, and then having the possibility to prevent, treat, and reverse these diseases is fundamental. It’s so important for our health, in particular.

Dale Bredesen, MD

It’d be a little bit like measuring insulin resistance and preventing diabetes. there’s a tremendous that you can do. Thank you very much. I want to mention that there will be a significant reduction. We’re working with the neural code now. There’ll be a significant reduction in cost through the Apollo website. I’m very excited about that. As I said, this is going to be the most important test that we do this year. As soon as this is completed and ready, I will be getting it myself because I want to know where I stand and make sure that, over time, I can do whatever is needed to make sure that I don’t undergo a neurodegenerative process. Dr. Hans Frykman, thank you so much for joining us. Are there any final words I’ve missed here on these tests that we should discuss?

Hans Frykman, MD, PhD

No, I don’t think so. No, not right now. This was very comprehensive. There’s a lot of information. of us that work with this deal is all-natural. But there’s a lot for people to process. I would like to encourage people to not hold back if they have questions. Please come forward with the questions. My emails can perhaps be displayed at the end of this talk, and we have a full-time neurologist with our company who is very experienced. You can ask me, there’s not a pathologist as well who has a PhD in AD and Alzheimer’s disease. so there are there is a backup for any practitioner who wants to ask questions to us. We want to serve everybody. and that people walk away with a good understanding of what these tests mean, with the help of Dale’s program, it would be helpful to get on the right track to know where you are at and how you improved. Then you have an objective measurement of how you are improving. This is very important.

Dale Bredesen, MD

Thank you. Again, thanks for all the great work you’ve done over the years, and thanks for developing these. Again, they are going to change lives. Thanks very much, Hans.

Hans Frykman, MD, PhD

It was my pleasure. Thank you.