Chapter 24: Drugs for Neurodegenerative Diseases

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Hello and welcome back to The Deep Dive.

Today, we are turning our attention to, well, one of the most intricate, fascinating, and frankly, emotionally heavy areas of medicine.

We are diving deep into the pharmacology of neurodegenerative diseases.

That's a massive topic.

We're looking at conditions where the nervous system, basically the central nervous system, progressively loses function.

And,

you know, it's not just about forgetting names or having a shake in your hand.

It's about the fundamental wiring of the brain breaking down.

Exactly.

And to guide us, we are relying exclusively on chapter 24 of Brenner and Steven's Pharmacology, sixth edition.

This text is our Bible for the next hour.

That's our map.

It is.

Our mission here is really specific.

We want to demystify the drugs used to treat these conditions.

We want to understand how a pill can, you know, attempt to fix a broken circuit in the brain.

And my job here is to make sure we keep the science grounded in that text.

Because when you talk about the brain, it's just so easy to get lost in theory or speculation.

But chapter 24 gives us a very structured pharmacological map of what we can actually do for these patients right now.

So let's lay out the landscape.

We're covering the big five today.

We've got Parkinson's disease, Huntington disease, Alzheimer's disease, multiple sclerosis, and amyotrophic lateral sclerosis, better known as ALS.

And we'll wrap up with a final section on spasticity, which often accompanies these disorders, particularly something like MS.

The text makes an important distinction right off the bat that I think we need to highlight.

It says that the signs and symptoms of these diseases do not reflect normal aging.

That is a crucial point.

Everyone forgets things as they get older and, well, everyone slows down physically.

But these diseases are pathologic processes.

Not the same thing.

Not at all.

The text highlights that while the exact quases are often unknown, we're looking at a mix of heredity, autoimmunity, and environmental factors.

These are distinct disease states, not just the result of getting old.

And the current reality, as the chapter admits, is a bit of a mixed bag, isn't it?

It is.

The text is very honest about this.

It states that we have substantial progress in drugs for Parkinson's and some for Alzheimer's.

But for the other neurodegenerative diseases, therapy is pretty limited.

So we're often treating symptoms.

We're often treating symptoms rather than the root cause.

Yeah.

However, the text also emphasizes that research is moving fast and our understanding of the pathways is getting better every single day.

Okay, so let's start with the condition where we arguably have the most pharmacological tools.

Parkinson disease.

The dopamine deficit.

Right.

When I think of Parkinson's, I think of the classic triad of symptoms.

The text lists them clearly.

Resting tremor, rigidity, and bradykinesia.

And it's worth breaking those down because the terminology really matters.

Resting tremor is that involuntary trembling you see when a limb is at rest.

It often looks like pill rolling where the thumb and forefinger sort of rub together.

I've seen that.

Yeah.

Rigidity is an increase in muscle tone, which leads to resistance to passive movement.

It just feels like stiffness.

And bradykinesia.

It simply means slowness of movement.

It's a difficulty in initiating movement.

Getting up from a chair, for example.

And physiologically, what is going wrong?

Where is the break in the wire?

It's deep in the brain, in an area called the basal ganglia.

Specifically, we're looking at the degeneration of dopaminergic neurons, neurons that produce dopamine.

Okay.

These neurons originate in the substantia nigra, and they project to other structures in the striatum.

When they die, that whole circuit fails.

Why do they die?

Does the text give us a why?

Well, it discusses the oxidative stress theory.

The idea is that the metabolic oxidation of dopamine itself yields free radicals.

Let's unpack that.

What exactly are free radicals?

They're highly reactive molecules.

They're missing an electron.

So they go around stealing electrons from other molecules, causing all sorts of cell damage in the process.

So the very chemical the brain uses for signaling dopamine might be creating toxic byproducts.

That's the theory that these byproducts eventually damage the very cells that are making it.

So it's almost like the engine is overheating and damaging itself.

That's a pretty good analogy.

The text suggests this oxidative damage might be a key driver in why these specific neurons degenerate.

To really understand how the drugs work, we have to visualize the wiring diagram.

The text refers to figure 24 .1, which maps out the basal ganglia.

I love this part because it explains movement like a car.

It's a great analogy.

The basal ganglia's job is to coordinate smooth movement, and you have two main pathways connecting the striatum to the thalamus.

The first one is the direct pathway.

Right.

Think of this as the gas pedal.

It's excitatory.

It tells the cortex, go ahead, move that arm.

And the second one.

That's the indirect pathway.

This is the brake.

It's inhibitory.

It tells the cortex, hold on, don't move just yet.

So in a healthy brain, the gas and brake are perfectly balanced.

What happens in Parkinson's?

Remember, dopamine is the modulator here.

Dopamine stimulates the direct pathway, the gas pedal via D1 receptors.

Okay.

And it inhibits the indirect pathway, the brake via D2 receptors.

So when you lose dopamine - You take your foot off the gas and you stop inhibiting the brake.

Exactly.

You lose the go signal and you amplify the stop signal.

So the brake gets slammed on.

That's a perfect way to put it.

That explains the rigidity and the inability to start moving.

You're just stuck with the brakes on.

And there's one more player to mention, acetylcholine.

Yes.

In the striatum, you also have these excitatory cholinergic neurons.

Normally, dopamine keeps them in check,

but when dopamine drops, acetylcholine activity becomes relatively excessive.

So it's a seesaw, dopamine goes down.

And acetylcholine is relatively up.

Exactly.

And that gives us our two main strategies for drugs, either boost dopamine to press the gas or block acetylcholine to release the brake.

Let's talk about the heavy hitter first, the gold standard, levodopa.

Levodopa, also known as L -dopa.

The obvious question is, if the brain is missing dopamine, why don't we just give the patient a dopamine pill?

It's a problem of access.

Dopamine itself, the molecule, does not cross the blood brain barrier.

So if you inject it, it'll affect your heart, your blood vessels, but it will never reach the brain cells that actually need it.

So levodopa is a kind of Trojan horse.

In a way, yeah.

Levodopa is a precursor.

It can cross the blood brain barrier using a specific transporter.

Once it's inside the brain, an enzyme called AAAD converts it into dopamine.

So it's called precursor loading.

Exactly.

We send in the raw materials, and the brain manufactures the finished product on site.

But getting it there isn't simple.

The text mentions some specific pharmacokinetic hurdles.

Oh, huge hurdles.

First, levodopa is absorbed in the duodenum, but it uses the same transport system as large neutral amino acids.

So dietary protein competes with the drug.

Yes.

So if you eat a big steak dinner, the amino acids from the steak are fighting the levodopa for a seat on the bus to get into the blood.

Exactly.

And that's why a protein restricted diet or just being careful about timing meals can sometimes really improve the response to the drug.

And then there's the first pass problem.

This is critical.

The text states that about 95 % of an oral dose of levodopa is metabolized in the gut and the liver before it ever reaches the systemic circulation.

95%.

Yep.

Enzymes in the body, that same AAAD enzyme and another one called COMT just chew it up.

Wait, so only a tiny fraction actually gets to the brain?

If you give levodopa all by itself, yes, maybe 1%.

Yeah.

Which is just terrible efficiency.

And all that dopamine created outside the brain.

That causes massive side effects.

Nausea, vomiting in like 80 % of patients.

Cardiac, it's a mess.

Which leads us to the dynamic duo,

levodopa's essential partner, carbidopa.

Carbidopa is the best friend levodopa ever had.

Figure 24 .2 in the text illustrates this perfectly.

Carbidopa inhibits that AAAD enzyme.

But wait, we need that enzyme to turn levodopa into dopamine inside the brain.

If carbidopa stops the enzyme, doesn't it ruin the whole point?

Ah, that's the genius of it.

Carbidopa does not cross the blood brain barrier.

So it inhibits the enzyme strictly in the body and the periphery.

It prevents levodopa from turning into dopamine in your gut and your blood.

So more of it survives the journey to the brain.

And what's inside the brain?

There's no carbidopa.

So the conversion happens exactly where we want it to.

That is clever.

It's like an armored truck that protects the money until it gets to the bank, but it doesn't go inside the vault.

Perfect analogy.

And because of this, you can lower the levodopa dose by about 75 % and you drastically reduce those nasty peripheral side effects like nausea and heart palpitations.

And that's why the combination drug, cinnamate, is the standard.

That's right.

Even with this combination, though, levodopa isn't perfect.

The text talks about effectiveness declining over time.

Sadly, yes.

Remember, levodopa needs functioning neurons to convert it to dopamine and then store it.

As Parkinson's progresses, more of those neurons die.

The factory is shutting down.

And that's when you start seeing fluctuations.

Exactly.

You see the wearing off effect.

What's that?

That's when the drug just stops working toward the end of a dose.

The patient gets stiff and slow before it's time for their next pill.

The storage capacity of the brain is just diminishing.

And the on -off phenomenon.

That's even more distressing, really.

It's unpredictable.

One minute the patient is moving fine, they're on.

The next minute they freeze up completely, they're off.

And it's not tied to the dose timing.

Not anymore.

The system is just becoming unstable.

We also have to mention the adverse effects of long -term use.

Dyskinesias.

These are peak dose dyskinesias.

Rithing, flinging movements of the arms or legs.

Sometimes chewing motions.

It looks like the patient is moving too much.

So it's the opposite of the bradykinesia.

It is.

It happens when dopamine levels spike too high.

So you have this very narrow therapeutic window.

Too little drug, and they are rigid.

Too much, and they have dyskinesia.

The text also warns about interactions.

Two big ones.

Vitamin B6.

It actually speeds up the breakdown of levodopa outside the brain, so it makes it less effective.

And the other.

MAOIs.

Specifically non -selective ones.

If you mix those with levodopa, you can get a hypertensive crisis.

A really dangerous spike in blood pressure.

Okay, so levodopa is the foundation.

But we have ways to make it work better.

Let's talk about the extenders, the COMT inhibitors.

Right.

We mentioned AAD is one enzyme that eats levodopa.

The other is COMT.

Drugs like tolkapone and antikapone inhibit COMT.

What's the difference between them?

It comes down to location and safety.

Tolkapone works in both the brain and the periphery.

It's very powerful.

But.

But.

There have been rare but serious reports of fatal liver toxicity.

So it requires strict monitoring of liver enzymes.

That sounds risky.

It is.

And that's why antikapone is often preferred.

It only works in the periphery.

It doesn't cross into the brain.

But it's safer.

No liver toxicity reports.

It just helps more levodopa survive the trip to the brain.

So antikapone basically extends the half -life of levodopa.

Exactly.

It makes each dose of levodopa last a little longer, which helps to smooth out that wearing -off effect.

Another way to keep dopamine levels up is to stop it from breaking down inside the brain.

That brings us to the MAOB inhibitors, selagelin and resagelin.

And we have to be specific here.

Yeah.

These inhibit monoamine oxidase type B.

Type B.

Right.

Type B is the one mostly found in the brain that breaks down dopamine.

So by blocking it, you keep the dopamine that's there in the synapse for longer.

The text has this incredible story about MPT -Key and the frozen attics.

Can we touch on that?

It's fascinating.

It's a tragic but scientifically pivotal moment.

Back in the 1980s, some people taking a designer street drug accidentally ingested a contaminant called MPTP.

And what happened to them?

The MPTP gets converted in the brain into a potent toxin called MPP plus egg rye.

This toxin selectively and rapidly destroys the substantia nigra.

These young people developed instant, permanent, severe Parkinsonism.

They were frozen.

Just like that.

Just like that.

It was devastating.

How does this relate to selagelin?

Well, the conversion of MPTP into that toxin requires the enzyme MAOB.

Studies showed that selagelin blocked that reaction.

If you gave selagelin, the toxin wasn't formed.

So that led to a theory.

It did.

The theory was maybe selagelin could be neuroprotective.

Maybe it could stop the natural progression of Parkinson's if it's caused by similar environmental toxins.

Is that theory proven?

It's controversial.

The text says some studies show it slows progression.

Others say it doesn't.

But it definitely helps with symptoms.

There's one weird note on selagelin.

It metabolizes into amphetamine.

It does, which explains why a side effect can be insomnia or jitters.

Taking it late in the day is a bad idea because it can keep patients awake all night.

Let's move to a drug that was a complete accident.

Amantadine.

The antiviral surprise.

It's an influenza drug.

But they noticed that patients who had Parkinson's got better while taking it for the flu.

And we figured out why.

It seems to increase dopamine release and also block its reuptake.

A kind of double whammy.

It has a very specific side effect mentioned in the text.

Levado reticularis.

Yes, a reddish -blue modeling of the skin, usually on the legs.

It looks like a lace or net pattern.

It isn't benign, but it can be alarming if you don't know what it is.

Okay, so far we've talked about saving dopamine or boosting the supply.

But what if the factory is totally burned down?

What if there are no neurons left to make dopamine?

Then you need dopamine receptor agonists.

These drugs skip the middle man entirely.

How so?

They don't need to be converted.

They don't rely on the dying neurons.

They just go straight to the receptor on the receiving nerve as a, Hello, I'm dopamine.

They stimulate it directly.

We have two classes here.

The old school ergot derivatives and the newer non -ergots.

The ergot derivative mentioned is bromocryptine.

It's rarely used now for Parkinson's.

And interestingly, the text notes, another ergot, pergolide, was pulled from the market for causing damage to heart valves.

So we mostly use the non -ergots.

Pramopexel, ropinerol, and the patch rhodogatine.

These are really fascinating drugs.

They're often used in early Parkinson's to try and delay the need for levodopa or in later stages to help smooth out those off times.

And they have a totally different indication too.

They do.

They're also used for restless leg syndrome.

But the side effects.

These are the ones with the impulse control warnings, right?

Yes.

Nausea and sedation are common, but the text makes a point to highlight that some patients develop really serious impulse control issues.

Compulsive gambling,

shopping, hypersexuality.

Why does that happen?

Well, it stimulates the brain's reward pathways a little too well in some people.

There's one more agonist, an injectable one,

epimorphine.

And despite the name, it is not an opioid.

It has nothing to do with morphine.

Okay, important clarification.

It's a rescue drug.

If a patient has a severe freezing episode where they can't move at all, an injection of epimorphine can act within minutes to get them moving again.

The big downside is that it causes severe nausea.

We focus entirely on dopamine, but remember the teeter totter.

If dopamine is low, acetylcholine is relatively high.

Right, so we can use anticholinergics, drugs like benestropine and trihexaphenadol.

How do they help?

They're particularly good at reducing the tremor.

By blocking acetylcholine, they try to restore that balance in the basal ganglia.

But blocking acetylcholine comes with a cost.

We call them the anti -celendee effects.

Exactly.

Dry mouth, urinary retention, constipation, confusion.

And in the elderly population, which is most Parkinson's patients, that confusion and memory loss can be a major problem.

So these drugs have to be used very cautiously.

Finally for Parkinson's, there are some brand new players listed in the adjunct section of the chapter.

Yes, a few interesting ones.

Istra Defiling, it's an adenosine A2 antagonist that helps reduce off time.

And pimavanserin, that one seems really important.

It is huge.

It treats the hallucinations and delusions of Parkinson's psychosis without blocking dopamine, which would just make the motor symptoms so much worse.

So how does it work?

It targets serotonin receptors instead.

It's a completely different approach.

And dextromethorphanquinadine.

That's for something called pseudobulbar effect.

You see this in PD, but also in ALS and MS.

It's this emotional lability, uncontrolled crying or laughing that doesn't match the person's actual mood.

This drug combination dampens that excitatory transmission.

Okay, that is a comprehensive look at Parkinson's.

Let's pivot to the other giant in this field.

Alzheimer disease?

The cholinergic crisis.

The text opens this section with box 24 .1, the case of the forgetful father.

It describes a 59 -year -old man, trouble finding words.

He missed his son's soccer game, which he never does, and he's getting agitated.

It's a heartbreaking, but classic presentation.

Pathologically, we're seeing cortical atrophy, neurofibrillary tangles, and neuritic plaques made of beta amyloid.

And on a neurotransmitter level.

The text emphasizes the destruction of cholinergic neurons in the basal forebrain, specifically a place called the minor nucleus.

These neurons are critical for memory.

They are.

So the primary pharmacological strategy is like the Parkinson's teeter totter, but in reverse, we have too little acetylcholine.

We need to boost it.

Enter the acetylcholinesterase or ACE inhibitors.

Acetylcholinesterase is the enzyme that eats acetylcholine in the synapse.

So if we inhibit the eater, the acetylcholine stays around longer and can work harder.

Who are the players here?

Dunpeazle is the most common.

It has a long half -life, so it's just once a day.

That's convenient.

Very.

Then there's rivastigmine, which is available as a transdermal patch for better compliance,

and galantamine.

The text mentions galantamine comes from daffodil bulbs.

Pseudo -narcissus.

It's amazing pharmacology so often starts in the garden.

What's the reality of these drugs?

Do they cure Alzheimer's?

No.

The text is very, very clear on this.

These are symptomatic treatments.

So they just manage symptoms.

They may slow the deterioration of cognitive function for a while, maybe give you six months to a year of better time, but they do not stop the underlying disease progression.

The neurons are still dying.

And side effects.

Since we are boosting acetylcholine, you'd expect the opposite of the Parkinson's anticholinergics.

And you'd be right.

Nausea, diarrhea, bradycardia, a slow heart rate.

Essentially the SLA -DGE effects.

There's one drug that works differently.

Mementime.

Yes.

Mementime is an NMDA receptor antagonist.

It works on the glutamate system, not the acetylcholine system.

What's the theory there?

The theory is called excitotoxicity.

The idea is that excessive glutamate stimulation is actually toxic to neurons.

It overexcites into death.

For mementime.

It sort of blocks this background noise and helps protect the neurons from that damage.

It's often combined with dunpasal for moderate to severe AD.

The text also briefly mentions a medical food called capryladine.

What's that about?

It's an interesting idea.

The theory is that in Alzheimer's, the brain loses its ability to process glucose efficiently for energy.

Capryladine is metabolized into ketone bodies, which can provide an alternative energy source for the brain when glucose utilization starts to fail.

Fascinating.

Let's move to Huntington disease.

This feels like the pharmacological opposite of Parkinson's.

In many ways it is.

Huntington's is an autosomal dominant genetic disorder.

Pathologically, what we're seeing is the degeneration of GABA neurons in the striatum.

And GABA is the main inhibitory neurotransmitter.

Right.

It's the brain's primary break.

So if you lose the inhibitor, you get disinhibition.

This leads to excessive dopaminergic activity, relatively speaking.

So in Parkinson's, we have low dopamine and not enough movement.

In Huntington's, we have relatively high dopamine and too much movement.

That Korea, those dance -like movements.

Exactly.

So the entire treatment strategy is to dampen the dopamine.

How do we do that?

The text highlights VMAT2 inhibitors, tetrabenazine and deutrabenazine.

These are clever drugs.

VMAT2 is a transporter protein.

Its job is to pack dopamine into vesicles, the little storage bubbles inside the neuron before release.

If you inhibit VMAT2, the dopamine isn't packed away safely.

It gets left out in the cytoplasm where it gets broken down by MAO.

So you are essentially emptying the amoclypse so the neuron can't fire as much dopamine.

That's a great analogy.

It depletes the mono means.

Less dopamine available for release means less Korea.

Are there other options for Huntington's?

Well, you can use anti -psychotics like haloperidol, which block dopamine receptors directly,

or benzodiazepines like Diazepam, which boost GABA.

But the VMAT2 inhibitors are really the specific approach for the Korea itself.

Next up is multiple sclerosis or MSK.

This is a different beast entirely.

It's an autoimmune disease.

Yes.

In MS, the body's own immune system attacks the myelin sheath, the fatty insulation around the nerves in the central nervous system.

This leads to inflammation, plaques and disrupted nerve signals.

The text breaks treatments into disease modifying therapies or DMTs and symptomatic management.

Let's talk about the DMTs.

These all seem to be about calming the immune system down.

That's the goal.

The first breakthrough was interferon beta 1B and beta 1A.

What do they do?

They're immunomodulators.

They reduce relapse frequency.

The mechanism seems to involve reducing inflammatory cytokines like interferon gamma.

Then there's gladeram or acetate.

I love the description of this one.

A myelin decoy.

It's a great description.

It is a synthetic protein that is engineered to look like myelin.

The idea is that the attacking T cells bind to the drug instead of to your actual nerves.

It basically acts as a sponge for the immune attack.

And for more aggressive cases, we have monoclonal antibodies, natalizumab.

Natalizumab blocks cell adhesion molecules.

Think of it like locking the doors to the brain.

It prevents the lymphocytes, the attack cells from crossing the blood -brain barrier and getting into the CNS where they can do damage.

And alintuzumab.

The text kind of presents that as the nuclear option.

It's a CD52 -directed cytolytic antibody.

What does that mean?

It binds to a protein called CD52 on immune cells.

And just destroys them.

It wipes out a significant portion of the immune army.

So it's reserved for patients who haven't responded to other drugs.

There's been a big shift toward oral drugs for MS, which must be huge for patients.

No more injections.

Absolutely.

Fingalimod is a fascinating one.

It's a sphingosine 1 -phosphate modulator.

That's a mouthful.

What does it do?

It traps lymphocytes in the lymph nodes.

It effectively creates a traffic jam so the immune cells can't get out into the blood to go and attack the brain.

And dimethylhumorate.

That one activates the NRF2 pathway, which is the body's natural response to oxidative stress.

It helps the cells survive that inflammatory environment.

What about managing symptoms?

Walking is a major issue in MS.

There's a specific drug for that.

Dalfampridine.

It's a potassium channel blocker.

How does that help with walking?

Well, by blocking potassium channels on the nerve, it enhances signal conduction through the damaged, demyelinated personal nerves.

It's the only drug that is specifically indicated to improve walking speed.

And for acute attacks.

The flare -ups.

High -dose corticosteroids, like prednisone.

They don't change the long -term course of the disease, but they can shorten the acute flare -up by dramatically reducing edema and inflammation.

Moving on to amyotrophic lateral sclerosis, ALS.

This is perhaps the most difficult diagnosis we're covering.

It is.

It's a progressive wasting of motor neurons.

The mind often stays sharp while the body fails.

It's just devastating.

The pharmacological options here are very limited.

Very.

We have Riluzol.

It was the first approved drug.

It inhibits glutamate release and also blocks sodium channels.

It's neuroprotective.

What is the actual benefit?

It's modest.

The text states it extends survival, or the time, to needing a tracheostomy by about three months.

Three months?

Yes.

It's something, but it's not a cure.

And a newer agent at Aurovone.

It's a free radical scavenger.

Basically an antioxidant that's designed to reduce oxidative stress on the neurons.

Again, the goal is to slow the damage, not reverse it.

Finally, let's cover the spasticity section.

This overlaps with MS, cerebral palsy, and stroke.

Right.

Spasticity is disordered muscle tone.

That's stiffness and spasms.

Baclofen is the name I hear most often.

Baclofen is a GABA -B receptor agonist.

It works in the spinal cord to hyperpolarize motor neurons, basically telling them to relax.

It can be given orally or, for severe cases, via a pump directly into the spinal fluid.

Then there's tizanidine.

That's an alpha -2 adrenogic agonist.

It works centrally, kind of like clonidine, to inhibit the motor neurons presynaptically.

Its main advantage is that it tends to cause less muscle weakness than some of the others.

And dantrolene.

This one is unique because it doesn't work on the nerves at all, right?

Correct.

Dantrolene works directly on the muscle fiber itself.

It blocks the release of calcium from the sarcoplasmic reticulum.

And without calcium, the muscle physically cannot contract.

And it has a very important dual use.

Yes.

It's the antidote for malignant hyperthermia, that rare, life -threatening reaction to certain types of anesthesia.

Last but not least, botox.

Botulinum toxin A.

We think of it for wrinkles, but in spasticity, it's a localized weapon.

You inject it into a specific muscle, and it blocks acetylcholine release at the neuromuscular junction.

Temporarily paralyzing that muscle.

It's great for focal spasticity, like a clenched fist or a stiff neck.

Okay.

Let's try to wrap our heads around this whole chapter.

What's the big picture here?

Well, if we look at the overarching theme,

pharmacology and neurodegeneration is all about trying to restore balance.

Right.

In Parkinson's, we are balancing dopamine and acylcholine.

In Huntington's, we are trying to tame dopamine.

In Alzheimer's and ALS, we are fighting glutamate excitotoxicity, trying to boost acetylcholine.

And MS.

In MS, it's the immune system versus the myelin sheath.

Every strategy is about reestablishing a lost equilibrium.

And the trend seems to be shifting.

We started with just symptom relief, you know, levodopa making you move better today.

Exactly.

Now, with the MS drugs especially and some of the newer agents, we are trying to actually modify the course of the disease.

Absolutely.

The text alludes to the future.

Things like gene editing, CRISPR for Huntington's.

We aren't there yet clinically, but understanding these fundamental pathways.

Oxidative stress, excitotoxicity, autoimmunity.

That is the roadmap to getting there, from bandages to cures.

It's a field where the science is incredibly complex, but the impact on human life is just massive.

I'd encourage you, if you're studying this, to really look at the drug tables in chapter 24, especially the interactions, because as we've seen, these drugs do not play nice with others.

Absolutely.

One wrong combination like a non -selective MAOI in levodopa or an MAOI in an SSRI can be incredibly dangerous.

That's a wrap for this deep dive into neurodegenerative pharmacology.

Thank you from the last minute lectures.

Stay curious.