Chapter 7: Life-Span Brain Development & Behavior

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Welcome back to the Deep Dive.

Today we are attempting something that quite honestly feels a little bit impossible.

We usually take a topic and try to get to the bottom of it, but today's topic is the bottom.

It's the foundation.

It's a machine that is allowing you to process the sound of my voice right now.

Which is a very meta way to start.

It is meta.

We are talking about the human brain,

but not just here's the brain, here's what it does.

We are doing a biography.

We are looking at the life cycle of, well, the most complex object in the known universe.

That's a really good way to frame it.

A biography.

Because the brain isn't, you know, a static object.

It's not like a liver or a kidney where it grows to a certain size and then just sort of sits there doing its job.

Right.

The brain is a process.

It's a construction project that never really ends.

Exactly.

We are calling this womb to tomb.

We are going to track this journey from the very first moment of fertilization through the absolute chaos of the womb, through childhood, the teenage years, which explains so much.

Oh, it explains everything.

And all the way to the eventual decline in old age.

And just to, you know, set the ground rules, we are basing this entire deep dive on chapter seven of behavioral neuroscience, the eighth edition.

This is the gold standard text.

So everything we discussed today is coming strictly from that biological roadmap.

No fringe theories, just the hard science.

And to kick this off, I want to tell you a story that the text opens with.

It's the story of a man named Michael May.

And I think this story just perfectly captures why this topic is so mind bending.

It's a famous case, a really important one.

So picture this.

Michael May is three years old.

He's a toddler and tragedy strikes.

He's involved in a chemical explosion.

It's horrific.

It destroys his left eye completely.

It damages the surface of his right eye so badly that he is effectively blind.

And at three years old, I mean, that's a critical moment.

Right.

So he grows up in darkness.

He can tell if it's, you know, high noon or midnight, but that's about it.

No shapes, no faces, no movement.

But Michael is clearly a resilient guy.

He doesn't let this stop him.

He starts a business.

He gets married and get this.

He becomes a champion skier, grind skiing.

That is, that's terrifying to even think about.

He used guides who would shout directions, but he was navigating the world using sound and touch.

He essentially built a whole life without vision.

But then fast forward.

Michael is 46 years old.

It's been over 40 years since the accident and medical technology has made a huge leap.

Doctors tell him, Hey, we can do a stem cell procedure.

We can clear up the scarring on your right eye.

It can fix the camera.

Exactly.

They could fix the hardware.

So he agrees.

They do the surgery.

The bandages come off and physically for the first time in four decades, light is streaming through a clear lens, hitting a healthy retina and sending signals up to his brain.

And this is the moment everyone expects the Hollywood ending, right?

The music swells.

He sees his wife's face, tears flow.

That's what I would expect, but that is not what happened.

And this is the puzzle.

Michael opens his eye and he sees, well, not nothing.

He sees a wash of colors.

He sees vague motion, but he looks at his wife and he can't tell who she is.

He looks at a cube and a sphere on a table and he can't tell which is which.

Unless they moved.

Right.

It was the key thing.

Yes.

If someone threw the ball at him, he could catch it.

But if it was sitting still, it was just visual noise.

In fact, on the ski slopes, he found the visual input so overwhelming and useless that he had to close his eye to ski safely.

He was better off blind.

And that just drives home the central theme of this chapter.

We tend to think that seeing happens in the eye, but the eye is just a sensor seeing the interpretation of that data that happens in the brain.

Right.

And because Michael lost his vision at age three, his brain had made a decision, a decision in a biological sense.

Yeah.

The brain is ruthless.

It operates on a use it or lose it economy.

When Michael was three, the visual cortex, part of the brain at the back of your head, the processes site, it stopped receiving data.

So the brain didn't just let that real estate sit empty.

It repurposed.

It repurposed it.

It pruned away the connections for recognizing 3d shapes and faces because they weren't being used.

So when the camera was turned back on 40 years later, the software was gone.

The brain had moved on.

And that is what we are unpacking today.

The idea that your biography, your experience physically becomes your biology.

The structure of your brain is a history of what you have done and what has happened to you.

That is heavy.

But to understand how that happens, we have to go back to the start.

We have to look at the blueprint because before we get to experience, we have to build the machine.

And the numbers here, honestly, they just sound made up.

They are staggering.

Truly.

We have somewhere around 80 billion neurons in a mature brain.

Is that right?

Yes.

80 billion.

And each one of those neurons connects to thousands of others.

We are talking about 100 trillion connections or synapses.

100 trillion.

To put that in perspective, that is more connections in one human head than there are stars in the Milky Way galaxy.

That's impossible to picture.

It is.

And every single one of those cells, every one of those connections originates from one single starting point, the fertilized egg,

the zygote.

Okay.

So take me to the starting line.

We have one cell.

The clock starts.

What happens?

Speed.

Pure, unadulterated speed.

Within 12 hours of fertilization, that single cell begins to divide.

One becomes two.

Two becomes four.

It's exponential.

Just immediately.

Immediately.

By the third day, you have a little cluster of cells that looks like a bunch of grapes.

It's tiny.

About 200 micrometers.

You'd need a microscope to see it.

Absolutely.

But within a week, this cluster starts to organize.

It forms three distinct layers.

This is like the first architectural decision the embryo makes.

You have the endoderm, the mesoderm, and the ectoderm.

And based on the reading, the ectoderm is the star of our show.

It is.

Ectoderm translates to outer skin.

And this is one of those weird biological facts.

The same layer of cells that turns into the skin on your arm also turns into your brain.

That's wild.

My nervous system is basically just internal skin.

In a developed male sense, yes.

They're siblings.

As this ectoderm layer thickens, it forms a flat oval plate.

Then ridges form on the edges of the plate, and a groove forms down the center.

Like a hot dog bun.

A little bit.

That's a good analogy.

That's the neural groove.

Eventually, the tops of the bun, the ridges, they curl up, and they fuse together.

And this turns the groove into a tube.

The neural tube.

Wow.

This is the ancestor of your entire central nervous system.

It sounds like origami.

It is biological origami.

And it's high stakes.

If that tube doesn't zip up correctly, you get severe birth defects like spina bifida.

But assuming it zips, the front end balloons out to become the brain, forebrain, midbrain, hindbrain.

The tail end becomes the spinal cord.

And the hollow center.

That stays hollow.

It becomes the ventricles, the fluid -filled caverns inside your brain.

Okay, so we have a tube.

But a tube isn't a brain.

A brain is dense.

It's packed with those 80 billion neurons.

When do they show up?

This is where the numbers get terrifying.

Once the neural tube is formed, the fetus enters a period of peak growth.

During this phase, the developing brain is generating roughly 250 ,000 new neurons every single minute.

Wait.

A quarter of a million.

Every minute.

Every minute.

For weeks on end.

That sounds impossible.

I mean, imagine trying to build a city where you have to construct 250 ,000 houses every minute.

The logistics alone.

It's a biological frenzy.

By the eighth week of

embryo.

The body is just an afterthought.

Everything is being poured into building the brain.

But it can't just be random, right?

You can't just have a pile of 250 ,000 cells appearing and hoping for the best.

There has to be a plan.

No.

It is highly orchestrated.

And neuroscientists, specifically detailed in this chapter, have broken this process down into six distinct stages.

And I think walking through these six stages is the best way to understand how we go from a tube to a thinking machine.

Let's do it.

Stage one.

This is the explosion we just talked about.

Neurogenesis.

Right.

Neurogenesis literally means the birth of neurons.

This happens in the ventricular zone.

Remember that hollow inside of the tube?

The fluid -filled part.

The lining of that hollow space is the factory floor.

The cells there go through mitosis cell division.

But here's a nuance that the book highlights, and it's important.

Neurons themselves don't divide.

Wait, what?

How does that work?

You don't take a neuron and split it into two neurons.

Once a cell decides, I am a neuron, it never divides again.

The cells that are dividing are precursor cells.

They're basically stem cells.

They divide and divide.

And eventually one of the daughter cells stops dividing and becomes a neuron.

The other one keeps on dividing.

That feels like a very permanent decision for that one cell.

It is.

And for decades, the dogma in neuroscience was that this factory shuts down at birth.

We used to tell students, you're born with all the neurons you will ever have.

Don't kill them because they don't come back.

I definitely heard that growing up.

Don't drink that beer.

You'll kill brain cells and they're gone forever.

Well, the alcohol part is still good advice, but the gone forever part is technically wrong.

The text confirms that we now know about adult neurogenesis.

We continue to make new neurons in very specific areas, like the olfactory organ for smell and the hippocampus.

The memory center.

Exactly.

And this is where we can give the listener some actionable news.

The text explicitly mentions that this adult neurogenesis is boosted by survival factors,

specifically exercise, environmental enrichment, and learning.

So when I go for a run or when I sit down to learn a new language, I'm not just toning my brain.

I'm actually stimulating the birth of new hardware.

You are.

You are technically engaging in stage one of neural development, even right now.

That is empowering.

Okay.

So the factory is running.

We have these baby neurons born in the center of the brain, but the brain isn't just a hollow tube anymore.

It has layers.

The thinking part, the cortex is on the outside.

Correct.

The cortex is the outer rind.

So how do the cells get from the center to the outside?

Do they just squish their way through?

This is stage two cell migration.

And honestly, it's one of the most beautiful processes in biology.

The brain builds its own scaffolding.

Scaffolding.

There are special cells called radial glial cells.

Imagine the brain is a sphere.

These cells sit in the center and extend long, thin fibers all the way to the outer surface.

They look like the spokes of a bicycle wheel.

So they're like ropes, guide ropes.

Exactly.

They're guide ropes.

The newborn neurons latch onto these glial ropes and literally climb them.

They pull themselves hand over hand from the dark center of the brain out to the surface.

That is an incredible image.

Billions of little cells just climbing ropes.

And they do it in a very specific order.

The cortex consists of six layers.

You'd think they would build layer one, the outside first, then layer two and so on.

Yeah, that makes sense.

But they do the opposite.

The brain is built inside out.

Explain that.

Why inside out?

The first wave of neurons climbs the rope and stops to form the deepest layer, layer six.

The next wave plombs up, climbs past the layer six cells and settles on top to form layer five.

The next wave climbs past both of them to form layer four.

So the newest cells have the longest commute.

Exactly.

They have to crawl over all their older brothers and sisters to get to the top.

This ensures that the outer layers, which are often the most complex in terms of connectivity, are fresh and sit on top of the foundation.

And what happens if they get lost?

What if they fall off the rope?

That leads to disaster.

The text mentions that disordered migration is a likely cause of many developmental issues, including schizophrenia.

If the cells aren't in the right zip code, the wiring diagram is fundamentally flawed from the start.

Okay.

So the cells have commuted.

They are in the right neighborhood, but right now they are just generic cells.

They don't know who they are yet.

Welcome to stage three.

Differentiation.

This is the identity crisis.

A cell has to decide, am I a child?

How do they decide?

Is it written in their DNA from the start?

That's the classic nature versus nurture question, right?

And the answer is fascinating.

The text compares two organisms to explain this,

the C.

elegans worm and well, us.

The worm again.

We always come back to the worm.

We do.

In the worm, differentiation is intrinsic.

It is hard coded.

We can point to a specific cell in a worm embryo and say, you will be a sensory neuron.

And no matter what happens, it will be a sensory neuron.

It's robotic.

It's destiny.

That humans aren't worms.

Faithfully.

In vertebrates like us, differentiation is largely extrinsic.

It's based on induction.

Essentially the cell looks at its neighbors.

The neighboring cells release chemicals that say, Hey, we're becoming visual cortex cells over here.

You should join us.

So it's cellular peer pressure.

It's exactly cellular peer pressure.

Everyone else is doing it, but this is crucial for our survival because it is flexible.

If a few cells die during development, the neighbors can say to a new arrival, Hey, we need you to fill this gap.

The worm can't do that.

If a worm loses a cell, that function is gone forever.

We have plasticity built in from the start.

That's a great design feature.

Okay.

Stage four, we have the cells.

They are in place.

They know what they are.

Now they need to talk to each other.

Synaptogenesis.

This is the wiring phase.

The neuron has to send out its axon, its output cable, to connect to a target.

Sometimes that target is right next door.

Sometimes it's all the way down the spinal cord.

And it's dark in there.

They don't have eyes.

How does an axon find its target?

This is my favorite mechanism in the chapter.

At the tip of every growing axon, there is a structure called a growth cone.

Think of it like a hand and extending from the fingers of this hand are fine thread -like extensions called filopodia.

These filopodia are constantly waving around sampling the environment.

They are, for all intents and purposes, sniffing for chemicals.

Sniffing.

Chemical sniffing.

The target cells, the ones waiting for a connection release chemical attractants, it's like the smell of a pie cooling on a windowsill.

The growth cone smells the pie and crawls toward it.

At the same time, other areas release repellents, essentially a bad smell that says, don't come here.

So the axon is navigating a chemical obstacle course, pulling itself toward the good smells and avoiding the bad ones.

Precisely.

And once the growth cone touches the target,

the synapse is formed.

Connection established.

So we are building connections.

Millions of them.

This sounds like we were building a supercomputer.

But then we hit stage five.

And this is where the story takes a dark turn.

Neuronal cell death.

Yeah.

I read this part three times.

You're telling me that after all that work, the explosion of the rope climbing, the chemical navigation, the brain just massacres its own cells.

It does.

In some regions of the brain, 20 to 50 % of the neurons that are born will die before the baby is even born.

Why?

That seems so incredibly wasteful.

Biology is usually efficient.

Why build a house just to burn it down?

It is efficient, but in a really Darwinian way.

Think of it like this.

You don't know exactly how many neurons you need to control a specific muscle because everybody's a little different.

So the brain overproduces.

It sends out way more troops than necessary.

And then?

Then the hunger games begin.

Seriously?

Seriously.

The target cells, the muscles or other neurons, release a chemical called the neurotrophic factor.

The most famous one is nerve growth factor, or NGF.

Think of NGF as food.

But the target only releases a limited amount.

Exactly.

So you have, say, a hundred neurons connecting to a target that only has enough food for 50.

The neurons compete.

The ones that make the best connections and suck up the most NGFs survive.

The ones that don't, they undergo apoptosis.

Apoptosis.

That's the technical term for cell death.

It's not just death, though.

It's suicide.

The cell realizes it's not getting enough food, so it activates a gene program that causes it to dissolve itself from the inside out.

It neatly packages up its own proteins and disappears.

That is ruthless.

It's the target theory.

It ensures that the size of the brain perfectly matches the size of the body.

If you have a huge arm, that arm releases more NGF, so more neurons survive to control it.

It's a self -tuning system.

Wow.

Okay.

So the survivors are left standing.

That brings us to the final stage.

Stage six.

Synapse rearrangement.

Or, as I like to call it, the grape porning.

We've thinned out the cells.

Now we need to sharpen the connections.

Just because a neuron survived doesn't mean all its connections are efficient.

It might be connected to five different things when it really only needs to talk to one.

The text had a graph for this figure, 7 .14, that I found really surprising.

It showed the density of synapses over time.

That graph blows people's minds.

It shows that the peak of synapse density, the moment in your life when you have the most brain connections, is not when you are a wise old sage.

It's when you are about one or two years old.

A toddler.

A toddler's brain is a messy jungle of connections.

Everything is connected to everything.

That's why toddlers are so sensitive to sensory input, but also so uncoordinated.

So what happens after age two?

The line on the graph drops like a stone.

From childhood through adolescence, we are losing synapses.

We are pruning.

We are cutting the wires we don't use to make the remaining circuits faster and more efficient.

Use it or lose it.

The ultimate.

Use it or lose it.

And here's the kicker.

This pruning doesn't happen everywhere at once.

It moves from the back of the brain to the front.

The visual cortex is pruned early, but the prefrontal cortex, the part right behind your forehead.

The CEO of the brain.

The CEO.

Judgment, impulse control, long -term planning.

That area is the last to be pruned.

It doesn't finish maturing until your mid -twenties.

Which explains teenagers.

It explains everything about teenagers.

A teenager has an adult body,

adult emotions, adult drives.

All coming from the deeper, earlier maturing parts of the brain.

But the breaking system,

the prefrontal cortex, is still under construction.

The wiring is still messy.

So when a teenager does something incredibly risky or stupid and you ask, what were you thinking?

The biological answer is, I wasn't.

Because the part of my brain that thinks about consequences hasn't finished the wiring phase yet.

Precisely.

It's not malice, it's neuroanatomy.

So we've covered the six stages of the neurons.

But we can't ignore the support staff.

The text has a whole section on glia, specifically myelination.

Right, we can't skip myelin.

If neurons are the wires, myelin is the insulation.

Like the rubber on a copper wire.

Exactly.

Certain glial cells wrap themselves around the axons.

This fatty sheath prevents the electrical signal from leaking out, which increases the speed of the signal by a massive factor.

It's the difference between dial -up internet and fiber optics.

It is.

And just like pruning, myelination happens in a sequence.

We myelinate our sensory areas first and our motor areas second.

Which makes sense.

A baby needs to see and hear before it can effectively reach out and grab.

And the text points out what happens when this goes wrong.

Multiple sclerosis.

Yes.

MS fans.

It's an autoimmune disorder where the body's own immune system attacks its own myelin.

It strips the insulation off the wires.

So the signal leaks.

Or just stops.

The signal slows down, becomes garbled, or stops entirely.

That's why MS patients have such a wide range of symptoms.

Blindness, numbness, paralysis.

It all depends on which wires lose their insulation.

It really shows how fragile this whole system is.

And speaking of fragility, the chapter dedicates a significant portion to developmental disorders.

Because this factory, this 250 ,000 cells a minute factory, can easily get disrupted.

The text categorizes these disruptions into two main buckets.

Extrinsic, which is environmental,

and intrinsic, which is genetic.

Let's talk about the extrinsic ones first.

The environment.

The most obvious one is oxygen, hypoxia at birth.

If that baby can't breathe, those energy -hungry neurons start dying immediately.

It's that critical.

And malnutrition.

The hunger winter example was haunting.

The Dutch famine of 1944.

Mothers who were starving during pregnancy gave birth to babies with significantly smaller brains.

The building materials just weren't there.

But the one we really need to dwell on, because it is entirely preventable, is fetal alcohol syndrome, FAS.

The text was very, very stark about this.

Alcohol is a neurotoxin.

It is.

And remember those radial glial cells?

The ropes that the neurons climb?

Alcohol disrupts that scaffolding.

If the mother drinks heavily during that migration phase, the ropes can dissolve or become disorganized.

The neurons try to climb, but the path is gone.

They end up in the wrong place, or they just die.

And the result, visually, is shocking.

The book has that picture, figure 7 .17.

It compares a healthy brain to an FAS brain.

The FAS brain is smaller.

That's called microcephaly.

But even worse, the surface is smooth.

It lacks the complex folds and gyri of a normal brain.

And often, the corpus callosum, the bridge between the left and right hemispheres, is missing entirely.

So the two halves of the brain literally can't talk to each other.

Right.

And that leads to the severe cognitive and behavioral deficits we see in these children.

It's just a tragedy of biology.

Then we have the intrinsic factors.

The genes.

Down syndrome.

Fragile X.

But there was one genetic disorder that actually gave me hope.

PKU.

Phenylketonuria.

Yes.

So this is a genetic disorder.

If a baby has it, they lack an enzyme to break down a specific amino acid found in food called phenylenine.

And if they eat it, it builds up in the brain and becomes toxic.

It causes severe intellectual disability.

So 50 years ago, this was a life sentence.

It was genetic destiny.

Exactly.

But today, it's a success story.

Every baby is tested for PKU at birth, that little heel prick.

If they have the gene, the doctors say, okay, put this child on a special diet.

No phenylenine.

And if they follow the diet?

The brain develops perfectly normally.

No disability whatsoever.

That is such a crucial point.

Having the bad gene didn't doom the child.

The outcome depended on the interaction between the gene and the environment, which in this case was the diet.

And that, my friend, is the perfect segue to the most mind -bending concept in this chapter,

epigenetics.

Epigenetics.

This is a buzzword, but the text defines it very specifically.

It is the study of factors that change gene expression without changing the DNA code itself.

I always struggle with this.

How can you change the gene without changing the DNA?

Think of your DNA as a massive instruction manual, a library of books.

Every cell in your body has the same library.

But in a skin cell, the how to be a skin cell chapter is open, and the how to be a brain cell chapter is glued shut.

Okay, that makes sense.

Epigenetics is the librarian.

It decides which pages are open and which are closed.

It uses chemical markers like bookmarks or Glut2 turned genes on or off.

And the wild part is that experience can control the librarian.

Yes.

And the study that proves this is the famous licking study with mice.

Okay, I have to admit, when I read licking study, I chuckled, are we really basing human neuroscience on how much a mouse licks its babies?

It sounds funny, but the mechanism is profound.

In mice, you have good mothers who lick and groom their pups constantly.

And you have bad mothers who are more inattentive who ignore them.

High licking versus low licking.

Researchers found that pups raised by high licking mothers grew up to be calm, brave, and handled stress well.

Pups raised by low licking mothers grew up to be anxious and fearful.

But surely that's just learning.

You know, if your mom is anxious and ignores you, you learn to be anxious.

That's what they thought.

So they did the key experiment.

They switched them.

They took pups born to bad mothers and gave them to good mothers to raise.

The foster experiment.

And guess what?

The pups grew up calm.

But here's the, so what?

They looked at the brains of these mice.

They looked at the DNA itself.

They found that the mother's licking, the physical sensation of care,

actually caused a chemical change in the pup's DNA.

It removed a metal group,

a chemical silencer, from the gene that controls the stress response.

Wait.

So the licking literally unglued the pages of the stress management genes.

Yes.

The experience of being cared for physically altered the gene expression.

And that change was permanent.

Those mice stayed calm for the rest of their lives.

That is actually kind of terrifying.

It means that neglect isn't just a bad memory.

It's a physical scar on your DNA expression.

Biography because biology.

Which brings us full circle back to Michael May.

We talked about how his vision didn't come back because his brain had moved on.

The text explains this using the concept of sensitive periods.

This is the use it or lose it window.

And to understand it, we have to talk about the kitten experiments.

These are always tough to hear.

They are.

But they are foundational to our understanding of vision.

Researchers do what's called monocular deprivation.

They've been patched over one eye of a kitten during the first few months of life.

Keeping it in the dark.

When they took the patch off, the eye itself is perfectly healthy.

The retina worked.

But the kitten was blind in that eye.

The brain refused to process the signal.

But if they patched an adult cat's eye...

Nothing happened.

The vision returned instantly.

This proved that there is a specific window of time, a sensitive period, where the brain is deciding which eye to listen to.

There is a graph for this too.

The ocular dominance histogram.

Figure 7 .23.

It's a bell curve.

In a normal brain, most neurons in the visual cortex are binocular.

They listen to both eyes.

So they sit in the middle of the curve.

But in the deprived kitten, the curve shifts completely.

Every single neuron in the visual cortex had rewired itself to listen only to the open eye.

It's a hostile takeover.

It is.

The open eye literally stole the brain space from the closed eye.

The axons from the open eye sprouted new branches and took over the territory.

And the rule governing this turf war is Hebbian synapses.

Donald Hebb.

Neurons that fire together, wire together.

And the inverse.

Neurons that are out of sync, lose their link.

Exactly.

The synapses are competing for those neurotrophic factors.

That chemical food we talked about earlier.

The active eye synapses are firing.

So they get fed and grow strong.

The patched eye synapses are silent, so they starve and wither away.

And this isn't just about kittens.

This is lazy eye in humans.

Amblyopia.

Yes.

If a kid has one eye that drifts, the brain starts getting double vision.

The brain hates double vision.

So it suppresses the signal from the drifting eye.

It effectively patches it internally.

And if you don't catch it early.

The brain permanently disconnects.

That eye becomes functionally blind.

That's why you see kids wearing a patch over their good eye.

We are forcing the brain against its will to listen to the bad eye before the sensitive period closes for good.

We are hacking the Hebbian synapses.

We are.

Exactly.

So Michael May lost his vision at age three.

That was right in the middle of his sensitive period for organizing faces in 3D shapes.

Correct.

The neurons that fire together, wire together.

But his neurons, for face recognition, never fired.

So they never wired.

They were pruned.

And 40 years later, you can't just grow them back.

The window had closed.

It's a tragic story, but it teaches us so much about how we are built.

Okay, we have to finish the journey.

We've gone from the womb through the explosion of growth, the pruning of adolescents, the sensitive periods of childhood.

Now we face the tomb.

Aging.

The decline.

The text mentions the shrinkage.

The brain actually loses volume as we get older.

It does.

After age 30 or so, the brain starts to slowly lose weight.

But the text makes a very specific point here.

It's not just overall shrinkage that matters.

It's where it shrinks.

The hippocampus.

Right.

In Figure 7 .25, they show a study comparing elderly people with good memory versus those with impaired memory.

The people with memory loss had significantly smaller hippocampi.

So protecting that structure is the key to a healthy old age.

It seems to be.

But sometimes pathology takes over, and we have to discuss Alzheimer's disease.

The most common form of dementia.

And the book gets really specific about what Alzheimer's actually looks like under a microscope.

It's not just forgetting things.

It's a physical destruction of the tissue.

It is profound atrophy.

The brain literally shrivels.

But if you look at the cellular level, you see the two killers.

The plaques and the tangles.

Explain the difference.

Senile plaques are made of a protein called beta amyloid.

These form clumps outside the neurons.

Think of it like trash piling up in the streets of a city, blocking traffic.

Okay.

And the tangles.

Neurofibrillary tangles are made of a protein called tau.

These form inside the neurons.

They are twisted filaments.

It's like the internal skeleton of the building collapsing.

So you have trash blocking the streets with amyloid and buildings collapsing from the inside with tau.

A grim but pretty accurate analogy.

And specifically, this destruction hits the basal forebrain.

These are the cells that produce acetylcholine, a key neurotransmitter.

When they die, the brain loses the ability to transmit signals effectively across the cortex.

The lights just go out.

That is bleak.

Does the text offer any good news at all?

It does.

And it connects back to everything we've talked about.

The concept of cognitive reserve.

What is that?

It turns out some people have autopsies that show a brain full of plaques and tangles.

Physically, they had Alzheimer's.

But when they were alive,

they had no symptoms.

Their memory was fine.

How is that even possible?

They had a high cognitive reserve.

Because they were physically active, socially active and mentally challenged throughout their lives, they had built up so many connections, so much redundancy that their brain could literally route around the damage.

So the use it or lose it rule applies until the very end.

Absolutely.

By learning, exercising and engaging with the world, you are building a buffer.

You are building a stronger, more resilient machine that can withstand the damage of aging for longer.

That is the ultimate takeaway for me from this whole journey.

It should be.

It's the most hopeful part.

So let's wrap this up.

We've covered a lot of ground.

We started as a single cell.

We watched it fold into a tube.

We saw 250 ,000 neurons explode into existence every minute.

We watched them climb ropes, fight to the death for food, and then prune back their own connections to become efficient.

We saw how experience from a mother's lick to a ray of light physically wires the genes and synapses.

And we saw how, in the end, we have to fight to keep those connections alive.

That is the biography of your brain from start to finish.

It makes me realize the brain I have right now sitting here talking to you.

It's not the same brain I had 10 years ago, and it's not the brain I'll have 10 years from now.

It is constantly changing, and that leads to my final thought for the listener.

We often use the phrase, it's in my DNA, as an excuse, as if our biology is a fixed destiny.

But Chapter 7 proves that is fundamentally wrong.

Your biography becomes your biology.

Every book you read, every run you take, every skill you practice, you are physically restructuring the machine in your head.

You are the architect.

That is a huge responsibility, but also a huge opportunity.

It is.

Well, on that note, I think my synapses are fully saturated for today.

I need to go let some of this consolidate.

And boost that neurotrophic factor.

I will.

This has been a deep dive into the lifespan of the brain.

A warm thank you from the Last Minute Lecture team for listening.

We'll catch you on the next dive.