Name: How to Slow Cognitive Decline | Dr. Peter Attia & Dr. Andrew Huberman
Uploaded: 2024-11-28T07:12:25.000Z
Duration: 15 min 29 s
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What is the story with neurodegenerative disease, Alzheimer's in particular?

Basic passive voice

And perhaps as importantly, how can we all slow our own cognitive decline irrespective of whether or not we get what is called Alzheimer's dementia?

So Alzheimer's disease is both the most prevalent form of dementia and the most prevalent neurodegenerative disease.

We're talking about roughly 6 million people in the United States have Alzheimer's disease.

That's one in, let's see, I mean, about 2% of the total population.

But that doesn't include those with mild cognitive impairment or pre-dementia or other forms of dementia.

And of course, the right metric is not what percent of the population, which of course includes children, things like that.

So is age the major risk factor for getting Alzheimer's?  We stay with glaucoma, a disease I'm much more familiar with because my lab worked on it for many years.

The biggest risk factor for getting glaucoma is age.

The greatest risk factor for cardiovascular disease is age.

The greatest risk factor for cancer is age.

We tend to not spend a lot of time talking about that because it's not a modifiable risk.

So, you know, we tend to focus on modifiable risk factors.

So what else can we tell you just to give you kind of lay of the land?

So the second most prevalent neurodegenerative disease would probably be Lewy body dementia followed by Parkinson's disease, although the rate of growth of Parkinson's disease is the highest.

So I think it would probably be most, you know, those three diseases we want to really be paying a lot of attention to.

As you know, there are a lot of other neurodegenerative diseases.

Every one of these things is devastating.

Like multiple sclerosis.  Multiple sclerosis, ALS, Huntington's disease.

Vascular dementia is not Alzheimer's dementia, but it produces comparable symptoms.

Each of these things, by the way, are slightly different.

It's a dementing disease, but it also has a movement component.

So it sort of sits on a spectrum that's sort of, you know, I mean, loosely halfway between Alzheimer's disease and Parkinson's disease.

We talked obviously about age being the number one risk factor.

Kind of not that interesting because you can't do anything about it.

So the real goal is as we age, what are we doing to reduce risk?

Well, let's start with an important gene.

The gene that everybody's heard of certainly came up a lot on the Limitless special where Chris Hemsworth was, you know, made the decision to reveal something that none of us expected when we started that whole series, which was that he ended up being homozygous for the ApoE4 isoform.

So maybe folks understand we have two copies of every gene.

So for gene X, you have copy that you got from your mom and copy that you got from your dad.

And the ApoE gene is kind of a unique gene in that it really, it has three different isoforms that are all considered normal.

So you have the E2 isoform, the E3 isoform, and the E4 isoform.

That's the one that we have historically had as far back as we can go.

We actually think the E4 isoform offered a lot of advantages back in the day.

It's a bit of a pro-inflammatory isoform and it certainly offered protection against infections, especially parasitic infections in the CNS, which would have been a really important thing to select for 200,000 years ago.

I mean, you have a blood-brain barrier, you have a thick skull.

I mean, I'm not calling, I'm not telling you you have a thick skull, but, but I mean, it just seems like parasites and other tissues would be an issue because what we're talking about here is brain disease.

Anyway, I don't want to take us off course.

It probably offered some protection outside of the brain as well.

Anyway, the, the E3 isoform I think showed up, God, I think 50,000 years ago.

And the E2 isoform showed up very recently, about 10,000 years ago.

Now, today we realize that there's a clear stratification of risk when it comes to Alzheimer's disease that tracks with those isoforms.

So because you have two copies, you basically have six combinations of how you can combine those genes.

You could be 2-2, 2-3, 2-4, 3-3, 3-4, 4-4.

The prevalence of them is basically as follows. 3-3 is now the most common. 3 is the most common.

So double 3 is 55-ish percent of the population.

The next most common is the 3-4, which is about 25% of the population.

And then after that, most things are kind of a rounding error.

So 2-3s and 2-4s would be the next most common. 4-4s are very rare.

And 2-2s are the rarest of them all. 2-2s are less than 1%. 4-4s are about 1-2%.

Very important point here is that the E4 genes are not deterministic.

So they're highly associated with the risk, but they're not deterministic.

There are at least three deterministic genes in Alzheimer's disease.

One is called PSEN1, another one is called PSEN2, and another one is called APP.

Those genes collectively make up about 1% of cases of people with Alzheimer's disease.

So they're fortunately very rare genes, but sadly they are deterministic.

Meaning if you have those genes, you do get Alzheimer's disease.

And what's perhaps most devastating about those genes is how early the onset is of the disease.

These are people that are usually getting Alzheimer's disease in their 50s.

Actually, she's spoken about this very openly, whose mom had one of these genes.

And she got Alzheimer's disease in her early 50s.

I think she might have made it into her 60s before she died.

But absolutely devastating consequences here.

Because I know about the hippocampal degeneration.

Hippocampus, of course, being an area of the brain important for learning and memory.

Do they lose breathing centers or cardiovascular control?

Usually what happens is it's sort of failure to thrive, aspiration, things like that.

So it's usually they just stop eating or they can't control secretions.

Or they really lose the ability to even sense pain in their body.

And therefore they'll get an ulcer and they don't realize it.

And it'll become cellulitic and they'll develop a horrible infection in response to it.

The reason I ask is every once in a while a news report will come out based on a legitimate case study where they'll do a scan on some person and discover that they're missing literally half their cerebral cortex.

Like huge chunks of brain and they're functioning relatively normally.

And so here we're talking about a neurodegenerative disease of relatively, it's widespread but there are a few hot spots, of course, in the brain that degenerate more profoundly than others and the people dying.

It extends to lack of peripheral awareness or control and then some acute injury or infection.

You mentioned earlier some of the controversy, right?

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