Question 20 is a strengthening question. We're going to be given an argument and our job is to make it stronger.

So this one takes the framework of a phenomenon hypothesis, right?

So some things we're going to observe something happening and then we're going to try to give an explanation for it as our conclusion.

So stroke's already over, right? We're monitoring your brain and you're still losing nerve cells.

So those patients also exhibited the highest levels of the protein glutamate in their blood.

So there's a positive correlation between post-stroke nerve cell loss positively correlated with protein glutamate in blood, in your blood, right?

So there's a positive correlation there. So glutamate, which like we have no idea.

I mean, now all we know is that glutamate is in your blood, floating around in your blood and it's a protein.

That's all we know, right? So there's a positive correlation here and with this.

So I think the argument is either going to go, it's going to pin the explanation for why people are still losing nerve cells on glutamate

or it's going to say, oh, it's not this, right? Something else, right?

Glutamate, which functions within nerve cells as a neurotransmitter.

Okay, so you got to be very careful here because in biology, if it's inherently unfamiliar territory,

every step along the way, you got to start paint, you got to paint the picture.

Otherwise, these words just float around in like the ether and you have no idea, right?

Like what nerve cells, where are your nerve cells, right? Your nerve cells are in your brain.

So usually glutamate functions within a nerve cell, right?

Look at where glutamate is now. It's in your blood, right?

You see, like normally it's supposed to be within your nerve cell, right?

It's not supposed to be outside the nerve cell in the blood, say.

It's okay. So it functions within the nerve cells, the neurotransmitter.

And if it leaks from a damaged or oxygen starved cell, see, if the cell is damaged or I presume dead, I don't know,

heavily damaged or dead, right? Like it breaks out of the nerve cell.

If glutamate does that within the nerve cell, it's a neurotransmitter.

But once it breaks out of the nerve cell, it can kill surrounding cells, right?

That's what we know. And look, there's a lot of glutamate floating around in your blood.

So from these phenomenon premises, we make the conclusion,

we make the hypothesis that thus glutamate leaking from damaged or oxygen starved nerve cells,

that's the cause of long term brain damage resulting from strokes.

That explains this, right? They explain this. So, I mean, they skipped us a couple of steps here, right?

But our job here is to come in and help this argument out.

Any neurotransmitter that leaks from a damaging or oxygen starved will damage.

Well, that doesn't help. That hurts, right?

Now I just all of a sudden learn about this neurotransmitter X,

which could compete with glutamate as the culprit for—because any neurotransmitter can damage, right?

So that's—A doesn't help. B says stroke patients exhibit a wide variety of abnormal chemicals in their blood.

It doesn't—I mean, I think A weakens quite a bit.

This one, I think, weakens a little less, right?

Because the idea is that maybe it's not some other neurotransmitter X that we know damages, right?

Maybe it's just some other random chemical Y, right?

Maybe that's what's—that's the culprit that's responsible for this, right?

Who knows? It certainly doesn't help.

Okay, so there are no other transmitters other than glutamate, but you got to be careful here.

Because, see, like we talked about a correlation with glutamate and this damage, right?

This damage, long-term damage, correlated glutamate.

And we are told that glutamate could, right?

That here's a—here's the mechanism by which it would kill—it could be responsible for the continued damage

because this is how it kills nerve cells, right?

And then we say, thus, it's this. It's definitely glutamate.

Well, I mean, just by localizing glutamate to be—to being the only neurotransmitter that leaks out,

that doesn't mean you've neutralized other potential non-neurotransmitter-related causes, right?

There's some chemical, for example. It could be some other chemical that causes this damage.

It could be a whole host of other things, other proteins that are non-neurotransmitters that cause the damage.

So just telling me that glutamate is the only neurotransmitter doesn't help

because we don't know what role the class of things called neurotransmitters has to play here yet, right?

Neurotransmitters could be entirely unrelated to this damage, right?

In which case, what does it matter that glutamate is the only neurotransmitter, right?

D says, leakage from damaged or oxygen-starved nerve cells, the only possible source of glutamate in the blood.

So there you go, right? This here, we—do we have glutamate in the blood? Yes, we do, right?

See, the premise allows us—affirms this bit.

So D tells us, look, if you find glutamate in the blood,

the only possible source is glutamate leaking from damaged or oxygen-starved cells, right?

And now what do we know about glutamate that leaks from damaged—see, it can kill surrounding cells.

See, now this—with answer choice D added in addition to the premises phenomenon here, right,

together, our conclusion becomes a much more powerful explanation, right?

It becomes much more likely that glutamate is the cause of long-term brain damage.

Yeah, but we already knew that, right? Like, that's what—glutamate comes from damaged, right?

Damaged cells, right? Nerve cells can—I mean, when they say damage here,

I guess the implication is that either lightly damaged, moderately damaged, heavily damaged, or near-dead damage, right?

But here it just says, oh, it can survive enough damage.

That was sort of already presumed, wasn't it? Like, we didn't presume you just died, right?

So I don't think E adds anything new.