Study Correlates Copper Intake and Alzheimer's in Mice
IRA FLATOW, HOST:
This is SCIENCE FRIDAY. I'm Ira Flatow. A telltale sign of Alzheimer's Disease is a buildup of amyloid plaque. Theories about why these plaques build up in the brain, well, no one really knows why. A new study has proposed a possible link, at least in mice, between copper in drinking water and the buildup of these plaques.
Copper is everywhere. It's in nuts, shellfish, vitamin supplements and in our drinking water. Do we need to start watching our copper consumption? Rashid Deane is lead author of the study published in the proceedings of the National Academy of Sciences. He's a research professor in the department of neurosurgery at the Center for Translational Neuromedicine at the University of Rochester Medical Center and lead author on the paper.
Welcome to SCIENCE FRIDAY.
RASHID DEANE: Thank you.
FLATOW: Now, you looked at a certain lipo-protein, a receptor, LRP-1 in this study. What does LRP-1 do in a healthy brain?
DEANE: Oh, LRP-1, it's a traffic lipid. It's a (unintelligible) transporter of that and I look specifically at this LRP-1 in the blood vessels of the brain, and this is because it's a major transporter of this amyloid, beta peptide from brain to blood. And that's why we looked at it.
FLATOW: And when you put copper in the drinking water of the mice, what did it do to this ability to clear that amyloid out?
DEANE: It reduced it.
FLATOW: It reduced the ability.
DEANE: Yeah, in mice.
FLATOW: In mice. And you're very careful to say mice because it has not been tried out in humans yet.
DEANE: No, no. No, this is a big jump; to extrapolate the data in mice to humans requires considerably more work. Therefore we should be very cautious about it.
FLATOW: And how much copper did you give the mice?
DEANE: Well, I mean we dosed the mice via the drinking water for convenience. Not that we think the water quality's poor or because of anything to do with copper piping. It's just a convenient way of dosing the animals. So we don't want to cause any alarm about those sources of copper at all. And back to how much we give them, we gave it 1/10 of the EPA maximum allowed for our water, drinking water.
FLATOW: Wow, 1/10 the amount. We also get copper from food, do we not?
DEANE: Yeah. We get lots of copper from out food and also we didn't alter the copper in the food chow given to the mice either. I mean, there's lots of copper in food and there's quite a lot, quite a lot more than the water. But I said, we didn't want to actually induce copper deficiency. We wanted to find what would be the effect of altering the copper that the animal consumes as a whole.
And water was a convenient source of that. And there had been some indication earlier dosing animals via their water, this sort of level of copper in rabbits, given lipids as well, cholesterol cause accumulation of amyloid-like proteins in the brain.
FLATOW: And it caused the accumulation of it.
DEANE: Yeah, I mean more of it was present in the brain.
FLATOW: Did you find that with your study also?
DEANE: Yeah. There was a tendency for the amyloid beta peptide to increase in the brain, which we interpret as meaning if it's not being transported out because of the defective transporter, then it will tend to accumulate in the brain. But that's not deposits of amyloid. That's peptide that's increased, and due, we believe, to a failure in the transport of it out of the brain.
FLATOW: So the copper created a failure in the transport mechanism of taking the amyloid out of the brain so it stayed there.
FLATOW: Is what you're saying.
DEANE: Yeah, yeah.
DEANE: Yeah. It's damaged by a process called oxidative stress. That's what we've shown anyway.
FLATOW: Is this something new?
DEANE: In the case of the effect on the transporter, yes. In the case of the observation that copper affects amyloid, no, because there had been that indication earlier and there have been indications that copper could cross react with amyloid and perhaps trap it in the brain, and that was done outside the body so we don't actually know how that occurred inside the body and inside the brain.
But there were these hints and there were these - there were controversies as well. Some say copper is good. Some say copper is bad. But I got into it to address that effect, whether copper is actually playing a role at all in Alzheimer's disease. And because I was aware of the blood-brain barrier there, the specialized blood vessels of the brain, which is there to restrict the movement of toxins into the brain, and so I wanted to find out what was the role of the blood-brain barrier in this whole process.
FLATOW: So you sort of have a double whammy here.
DEANE: Yeah. The double whammy process is because when we dosed a mouse model (unintelligible) we found, quite surprisingly, that in addition to the copper accumulated in the blood vessels of the brain, those would tend to increase in the brain itself. And that, again, we were surprised to see that that sort of level caused an increase in the production of (unintelligible) hence the double whammy effect.
FLATOW: So you're not telling people not to consume copper. It would be almost impossible.
DEANE: No, definitely not. (Unintelligible) very cautious. Copper is very good for you. And similarly, I'm not saying to even not to be critical of their drinking water and copper because it's good. I'm taking the same water as well. And not to worry about the copper piping either, because I have copper piping as well.
FLATOW: So what use can we make then of what you've discovered?
DEANE: Well, I think maybe we need to address where we are reading, I think - I mean first we did it in mice and so we have to see what happens in humans. But if this were to be extrapolated to humans, then we have to get concerned about it, the total amount of copper we are taking in and see whether that plays a role. Is a case of too much of a good thing is bad?
FLATOW: Yeah. So how do you go and extrapolate to humans then? 'Cause you wouldn't be doing the mice studies if you weren't going to be leading to humans.
DEANE: Yeah, yeah. Well, we need to analyze more samples from humans and see where that takes us now. I mean, it's very much more difficult to study humans as you appreciate. This disease developed in many years, 65 and greater, and most develop it in their 70s probably. And that's a long period of exposure to copper to study.
And the fact of a (unintelligible) of exposure to more copper on this whole disease process, it's difficult to say when it really takes such a long time to develop Alzheimer's disease. Perhaps it's a cumulative process that over a long period of time, exposed too many toxins, this may do harm to the blood-brain barrier. And like so much toxins, if copper is a powerful oxidant, and maybe the balance between antioxidants and oxidants that's required over a long period of time.
FLATOW: So you've made a discovery that really is not easy to verify.
DEANE: (Unintelligible) other studies? Perhaps, yes. We have to think more seriously of how to do this. I mean it's an initial study which is needed, because we can't jump straight away and study in humans. So it's a good model to try to tease out what might happen now in humans.
DEANE: It's a first step.
FLATOW: It's a first - so what would be the second step?
DEANE: Well, to try something in humans and do some studies in humans, look at the correlation between copper more. It's been happening earlier as well. There is actually - some data suggests there is a link, some say there is not a link, and some said almost the reverse, a high level of copper may contribute to Alzheimer's disease and some have suggested the reverse; low levels of copper may contribute to it.
FLATOW: So you're just saying this is a preliminary study and somebody take it and run with it.
DEANE: Yes. We all need to think about it now. I mean, the data is there now so we need to think what it actually means for Alzheimer's Disease, which is a human disease and try to (unintelligible) of it.
FLATOW: Well, Dr. Deane, thank you for taking time to be with us today.
DEANE: Thank you.
FLATOW: Dr. Rashid Deane is lead author of the study published in the Proceedings of the National Academy of Sciences, research professor in the Department of Neurosurgery at the Center for Translational Neuromedicine at the University of Rochester.
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