December 9, 2025 • 13 mins
We map how Alzheimer’s disrupts the brain’s wiring, how symptoms progress from memory slips to loss of judgment and orientation, and why ruling out treatable look-alikes can change the story. We also weigh proven medications, cautious new therapies, and the daily practices that protect function and dignity.
• biology of plaques, tangles, and acetylcholine loss
• early, middle, and late symptom patterns
• risks that rise with age, family history, and genes
• diagnosis built on history, cognitive tests, and imaging
• reversible mimics including B12 deficiency and hypothyroidism
• cholinesterase inhibitors and memantine for symptom management
• monoclonal antibodies, potential benefits, and MRI-monitored risks
• lifestyle strategies: exercise, cognitive activity, Mediterranean-style diet
• caregiver playbook: familiar routines, safe home, music and art engagement
This podcast is created by Ai for educational and entertainment purposes only and does not constitute professional medical or health advice. Please talk to your healthcare team for medical advice.
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Transcript
Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
SPEAKER_01 (00:00):
Welcome to the deep dive.
Today we're tackling a subjectthat is often incredibly complex
and for many deeply personal,Alzheimer's disease.
SPEAKER_00 (00:10):
Aaron Ross Powell It really is.
SPEAKER_01 (00:11):
We've pulled our information from some crucial,
very detailed source materialfrom experts at Harvard Health
because we know you want toapproach this with real
knowledge, but without gettinglost in all of the medical
jargon.
SPEAKER_00 (00:23):
Aaron Powell That's right.
And our goal for this deep diveis well, it's pretty clear.
We want to move beyond just thebasic definition.
We're going to try and unpackthe biological progression of
Alzheimer's or AD and uh clarifythe diagnostic methods, which
can be tricky.
SPEAKER_01 (00:38):
Aaron Powell And then get into the really current
stuff, the treatment andprevention strategies that are
evolving so quickly.
SPEAKER_00 (00:43):
Exactly.
SPEAKER_01 (00:44):
So AD is the most common form of dementia.
Our sources define it as anirreversible loss of brain
functions that just getsprogressively worse over time.
It typically starts after age60, but what is actually
happening inside the brain totrigger this collapse?
SPEAKER_00 (00:59):
Aaron Powell At its core, it's a tragedy of
communication failure within thebrain.
The very first function that'salmost always affected is
short-term memory.
SPEAKER_01 (01:08):
Aaron Powell That mental filing system you use
every minute.
SPEAKER_00 (01:10):
Aaron Ross Powell Exactly that.
The one that lets you recallwhat you just heard or where you
put your keys a second ago.
As that starts to erode, it umit gradually impairs other
intellectual abilities.
SPEAKER_01 (01:22):
Aaron Powell So things like language, problem
solving.
SPEAKER_00 (01:24):
Trevor Burrus Yes.
And eventually it leads toseverely impaired judgment.
SPEAKER_01 (01:28):
Aaron Powell So we know the result is this
intellectual failure, but let'sdig into the biology.
What's the cause of thissystem-wide failure?
The sources seem to point toboth a physical and a chemical
breakdown.
SPEAKER_00 (01:38):
Aaron Powell Absolutely.
SPEAKER_01 (01:39):
Yeah.
SPEAKER_00 (01:40):
And what makes AD such a well such a challenging
puzzle is that we don't have onesingle undisputed trigger.
What researchers haveidentified, though, are two
primary culprits.
Two proteins?
Two proteins that startaccumulating in, frankly, toxic
amounts.
They essentially begin tosuffocate the brain's
communication network.
SPEAKER_01 (01:59):
Aaron Powell Okay, and this is where we need to
give you the specificvocabulary.
It's not just two proteins, isit?
SPEAKER_00 (02:03):
Correct.
So the first protein is calledamyloid beta.
When it builds up too much, itforms these dense, sticky
clusters outside the braincells.
SPEAKER_01 (02:12):
And these are the famous plaques?
SPEAKER_00 (02:13):
These are the plaques.
You can think of them like, Idon't know, massive road
construction that justcompletely jams up all the
neural traffic.
SPEAKER_01 (02:19):
Okay, that's a clear image.
And the second protein.
SPEAKER_00 (02:21):
The second is tau.
And this one is different.
It starts twisting into theseabnormal fibers inside the brain
cells, and that forms what wecall neurofibrillary tangles.
SPEAKER_01 (02:32):
So if the plaques are traffic jam outside the
cell.
SPEAKER_00 (02:36):
Then the tangles are internal structural damage.
It's like the support beams ofthe cell twisting and buckling
until the whole structure justcollapses from within.
SPEAKER_01 (02:44):
Wow.
So it's a physical traffic jamoutside and a structural failure
inside.
That's devastating.
SPEAKER_00 (02:50):
That's the physical component, yes.
But we also see a chemicalproblem.
Our sources r really emphasizethe role of acetylcholine.
SPEAKER_01 (02:58):
Which is a neurotransmitter.
SPEAKER_00 (03:00):
A critical one.
It's basically the chemicalmessaging service between brain
cells.
In patients with AD,acetylcholine levels just
plummet, which makes thecommunication failure from the
plaques entangles even worse.
SPEAKER_01 (03:11):
Aaron Powell So you have a physical block and a
chemical shortage.
SPEAKER_00 (03:14):
Exactly.
And the um the end result ofthat double whammy is that the
brain cells themselves start toshrivel and eventually they die.
SPEAKER_01 (03:22):
Aaron Powell Before we track how this looks from the
outside, the symptoms, let'sjust quickly touch on who is
most susceptible.
What does the research say aboutrisk factors?
SPEAKER_00 (03:31):
Aaron Ross Powell The risk factors are uh pretty
crucial for understanding thewhole landscape.
The biggest one, notsurprisingly, is simply
increasing age.
The risk just climbsdramatically after 65.
SPEAKER_01 (03:42):
And there's a family connection?
SPEAKER_00 (03:44):
Strong one.
Having a parent or a siblingwith AD significantly raises
your personal risk.
And then finally, there arecertain specific genetic factors
you can inherit that just makeyou more vulnerable.
SPEAKER_01 (03:53):
Okay, so let's connect that internal biology to
the outward experience.
AD is progressive.
The symptoms follow this, well,this distinct and often
heartbreaking timeline.
How do the sources break downthe stages?
SPEAKER_00 (04:05):
We can draw a pretty clear line between the early
stages, where a person can stillbe surprisingly independent, and
the later, more debilitatingstages.
SPEAKER_01 (04:14):
So what does that early phase look like?
SPEAKER_00 (04:17):
In the earliest phase, the challenges are almost
all focused on acquiring newmemories and trying to retain
new information.
SPEAKER_01 (04:24):
So they might repeat stories or forget a conversation
they just had?
SPEAKER_00 (04:29):
Precisely.
Or struggle to learn a newrecipe, something like that.
SPEAKER_01 (04:32):
So if they're forgetting what they had for
breakfast, that's early stage.
But they can still, say, buttontheir own shirt.
SPEAKER_00 (04:38):
That is the crucial nuance right there.
A person in early AD usuallyretains their ability to manage
their daily physical needs.
They can feed themselves, bathe,dress, groom, all without
assistance.
SPEAKER_01 (04:51):
The operating system is failing, but the hardware,
the motor functions, they'restill working.
SPEAKER_00 (04:56):
A great way to put it.
The basic self-care is stillintact.
SPEAKER_01 (04:59):
So when does that change?
When does the deterioration moveinto those middle and later
stages?
SPEAKER_00 (05:03):
Aaron Powell That's when the brain's executive
functions really begin tocollapse.
The loss shifts from just newmemories to the gradual erasure
of older, more distant memories.
SPEAKER_01 (05:13):
And this is where complex tasks become impossible.
SPEAKER_00 (05:16):
Exactly.
Things that require planning insequence: managing a budget,
preparing a meal with multiplesteps, or just remembering the
sequence of taking dailymedication.
SPEAKER_01 (05:26):
And I know a big one for caregivers is the loss of
spatial awareness.
SPEAKER_00 (05:30):
It is a huge source of anxiety.
The sources highlight the dangerof losing your sense of
direction, even in a placethat's completely familiar, like
your own neighborhood.
SPEAKER_01 (05:39):
Or even your own house.
SPEAKER_00 (05:40):
Yes, it's a profound loss of that internal map we all
have.
SPEAKER_01 (05:43):
And beyond memory and function, the psychological
and behavioral changes seem, Imean, they seem just as
devastating.
SPEAKER_00 (05:50):
They often are for everyone involved.
We frequently see personalitychanges, um, things like
irritability, escalatinganxiety, or really profound
depression in the earlierphases.
SPEAKER_01 (06:01):
But it gets more severe.
SPEAKER_00 (06:02):
It does.
As the disease moves into themiddle and late stages, these
symptoms can escalate prettyseverely.
SPEAKER_01 (06:08):
We're talking about delusions and hallucinations
here.
That must be incrediblydifficult to manage.
SPEAKER_00 (06:13):
Incredibly.
Delusions are these irrationalbeliefs.
A patient might sincerelybelieve someone is stealing from
them or that they're beingpersecuted.
Hallucinations are sensoryexperiences that just aren't
real seeing or hearing things.
SPEAKER_01 (06:27):
And this can lead to things like aggression.
SPEAKER_00 (06:30):
It can, and it's often combined with a very
dangerous tendency to wanderaway from home.
It just requires immense,constant protective care.
SPEAKER_01 (06:38):
Aaron Ross Powell That thought, that level of
cognitive distress really bringshome how difficult this
diagnosis must be, which iswhere we should go now.
Let's unpack this.
The affected person oftendoesn't recognize there's a
problem, right?
They might even deny it.
SPEAKER_00 (06:51):
It's very common, yes.
SPEAKER_01 (06:52):
So how is a diagnosis of AD actually
reached?
It must rely so heavily onfamily and friends.
SPEAKER_00 (06:58):
It absolutely does.
The diagnosis really relies onthe history gathered from the
people who see the person everyday, the ones who can report on
memory lapses, poor judgment, orpersonality changes.
The family is the cornerstone.
SPEAKER_01 (07:10):
And the big challenge, which are sources
stress, is that there is nosingle definitive test for
Alzheimer's.
You can't just get a blood testthat gives you a yes or no.
SPEAKER_00 (07:18):
That is correct.
The diagnosis is clinical.
It's built on, well, onexclusion and compiled evidence.
A doctor will start with amedical history, a physical and
neurological exam, and what'scalled a mental status exam.
SPEAKER_01 (07:31):
Simple cognitive tests.
SPEAKER_00 (07:33):
Right.
Simple tests involving visualtasks, writing, and memory
checks.
SPEAKER_01 (07:37):
Aaron Powell But, and this feels like the most
critical part of this sectionfor anyone listening.
Before a doctor even considersan irreversible diagnosis of AD,
they have to rule out otherconditions that can look just
like it.
SPEAKER_00 (07:48):
This step is profoundly important.
It is, frankly, the only chancefor a truly treatable,
reversible diagnosis.
SPEAKER_01 (07:55):
Aaron Powell And what's fascinating is that the
sources pinpoint two specificconditions that can perfectly
mimic AD symptoms.
SPEAKER_00 (08:01):
They can.
And if they're caught, theoutcome is completely different.
We're talking about very lowlevels of vitamin B12 or a very
underactive thyroid, also knownas hypothyroidism.
SPEAKER_01 (08:10):
Wait, so a vitamin deficiency or a thyroid issue
can cause cognitive declinesevere enough that it looks like
Alzheimer's?
SPEAKER_00 (08:17):
That is precisely the danger and also the hope.
The incredibly importanttakeaway for you is that the
memory and thinking problemsfrom these issues can improve
and even go away entirely withtreatment.
SPEAKER_01 (08:29):
Wow.
So if a doctor skips that step,those simple blood tests.
SPEAKER_00 (08:32):
They might unnecessarily doom a patient to
an irreversible diagnosis whenthe real problem is entirely
fixable.
SPEAKER_01 (08:39):
That makes the blood work just about the most
important tool in the wholeprocess.
It's like checking the oilbefore you declare the engine is
broken for good.
SPEAKER_00 (08:46):
A perfect analogy.
So if those simple tests comeback clean, but cognitive
problems are still there, what'snext?
SPEAKER_01 (08:53):
Right.
What's the next step?
SPEAKER_00 (08:55):
They might move on to more detailed
neuropsychological testing,which is a much deeper dive into
cognition, and they'll almostcertainly order brain imaging
studies, a CT scan or an MRI.
SPEAKER_01 (09:05):
But it's vital to understand what these scans can
and maybe more importantly,cannot do.
SPEAKER_00 (09:10):
Yes.
They cannot diagnose AD withcertainty.
SPEAKER_01 (09:13):
But they rule other things out.
SPEAKER_00 (09:14):
Exactly.
They are critical for ruling outother structural causes, things
like a brain tumor or evidenceof a stroke.
The scans can show brainshrinkage or atrophy, which
supports a clinical diagnosis ofAD, but it's still not
definitive proof.
SPEAKER_01 (09:29):
And the diagnosis is usually confirmed by a
specialist.
SPEAKER_00 (09:32):
Yes, after referral to a neurologist, a
geriatrician, or maybe ageriatric psychiatrist.
SPEAKER_01 (09:38):
Aaron Powell So the picture is clear.
AD is irreversible.
Function declines until death.
The goal has to shift entirelyto management.
What do the sources say aboutproviding some hope, both in
delaying the onset and slowingit down once it starts?
SPEAKER_00 (09:51):
Let's start with prevention, or maybe more
accurately, delaying the onsetof symptoms.
The evidence we have stronglysupports simple lifestyle
factors that you can controlright now.
SPEAKER_01 (10:01):
Like staying active.
SPEAKER_00 (10:03):
Staying physically and mentally active is key.
Regular physical exercise,particularly aerobic exercise,
seems to be very protective.
SPEAKER_01 (10:10):
And diet always comes up in these conversations.
SPEAKER_00 (10:12):
He does.
The sources specificallyhighlight a dietary pattern,
kind of like a Mediterraneanstyle.
They emphasize a diet withplenty of fish, olive oil, and
lots of vegetables.
SPEAKER_01 (10:21):
So this is about delaying onset and maybe slowing
progression.
SPEAKER_00 (10:25):
It seems to be, yes.
It just underscores that what'sgood for your heart and your
vascular health is also reallygood for your brain.
SPEAKER_01 (10:31):
Okay, let's shift to treatment for those already
diagnosed.
What are the workhorse drugsthat aim to slow the decline?
SPEAKER_00 (10:38):
For mild to moderate AD, we rely on a class of drugs
called cholinesteraseinhibitors.
Now, since we saidacetylcholine, the brain's
messenger, is in short supply.
SPEAKER_01 (10:48):
Right.
SPEAKER_00 (10:49):
These drugs work by inhibiting the enzyme that
breaks it down.
SPEAKER_01 (10:52):
So you're basically preserving what little of the
messenger chemical is left.
SPEAKER_00 (10:55):
That's a great way to think about it.
You're helping the brain makethe most of its existing supply.
For moderate to severe AD,there's also a drug called
mementine, which works a bitdifferently to help stabilize
memory.
SPEAKER_01 (11:07):
And now we have to talk about the newer, more
complex therapies, the ones thathave been all over the news.
This is where we need to becautiously optimistic.
The monoclonal antibodies.
SPEAKER_00 (11:18):
We are.
We're talking specifically aboutaducanimab, aduhelm, and the
newer one, Lacanimab, um,Gipsula.
Both got accelerated FDAapproval.
SPEAKER_01 (11:27):
And unlike the other drugs that just manage symptoms,
these are designed to attack theunderlying problem.
SPEAKER_00 (11:33):
Exactly.
They target and try to clear outthose amyloid beta protein
deposits we talked aboutearlier, the plaques.
SPEAKER_01 (11:39):
The hope being if you clear the plaques, you might
slow or even halt the disease'sprogression.
But the sources are very clearthat we have to stress the
caution around these drugs.
SPEAKER_00 (11:50):
We absolutely must.
While they represent a huge leapforward in targeting the disease
mechanism itself, they come withsignificant risks.
The main concern is somethingcalled amylaid-related imaging
abnormalities or ARAA.
SPEAKER_01 (12:03):
ARAA, and what is that?
SPEAKER_00 (12:05):
It refers to side effects you can see on brain
scans, specifically brainswelling or microhemorrhages,
tiny little bleeds in the brain.
SPEAKER_01 (12:12):
That sounds extremely serious.
SPEAKER_00 (12:13):
It is.
Patients on these drugs have tobe monitored with regular MRI
scans to catch these thingsearly.
It really turns the treatmentdecision into a very careful
risk versus reward calculation.
SPEAKER_01 (12:24):
So beyond the pharmaceuticals, supportive
non-drug care is stillabsolutely essential.
SPEAKER_00 (12:29):
It's paramount.
The supportive environment iseverything.
Caregivers need to maintainfamiliar surroundings, people,
and routines.
Too much change can triggerconfusion and agitation.
SPEAKER_01 (12:40):
And creating safe environments to manage things
like laundering.
SPEAKER_00 (12:43):
Critical.
And also making sure the patientstays engaged, even as their
abilities fade.
SPEAKER_01 (12:48):
Through things like music or art therapy.
SPEAKER_00 (12:51):
Precisely.
Music, art, occupationaltherapy.
They all provide essentialstimulation and can offer real
emotional outlets.
It really takes a whole team.
SPEAKER_01 (12:59):
This deep dive has really given us a much clearer
picture of AD from the biologyof plaques and tangles all the
way to the cutting edge of thesenew, if controversial,
therapies.
SPEAKER_00 (13:08):
I hope so.
SPEAKER_01 (13:09):
And I think most importantly, we've highlighted
that critical need for a properdiagnosis, making sure to rule
out treatable conditions like aB12 deficiency or thyroid issues
before accepting thatirreversible diagnosis.
SPEAKER_00 (13:21):
Alzheimer's remains a severe challenge, there's no
doubt.
But this kind of informedapproach, combining lifestyle
efforts, early and comprehensivediagnosis, and the uh the
careful use of moderntreatments, that offers the most
critical path forward.
SPEAKER_01 (13:35):
And that leaves us with a final provocative thought
for you to consider as youreflect on all this.
If optimized lifestyle choices,physical and mental activity,
diet, and exercise, arescientifically shown to delay
the onset of symptoms and slowdisease progression later in
life, how much earlier in lifedoes the compounding biological
benefit of an optimizedlifestyle truly begin?
(13:56):
Something for you to mull overuntil our next deep dive.
Welcome to the deep dive.
Today we're tackling a subjectthat is often incredibly complex
and for many deeply personal,Alzheimer's disease.
SPEAKER_00 (00:10):
Aaron Ross Powell It really is.
SPEAKER_01 (00:11):
We've pulled our information from some crucial,
very detailed source materialfrom experts at Harvard Health
because we know you want toapproach this with real
knowledge, but without gettinglost in all of the medical
jargon.
SPEAKER_00 (00:23):
Aaron Powell That's right.
And our goal for this deep diveis well, it's pretty clear.
We want to move beyond just thebasic definition.
We're going to try and unpackthe biological progression of
Alzheimer's or AD and uh clarifythe diagnostic methods, which
can be tricky.
SPEAKER_01 (00:38):
Aaron Powell And then get into the really current
stuff, the treatment andprevention strategies that are
evolving so quickly.
SPEAKER_00 (00:43):
Exactly.
SPEAKER_01 (00:44):
So AD is the most common form of dementia.
Our sources define it as anirreversible loss of brain
functions that just getsprogressively worse over time.
It typically starts after age60, but what is actually
happening inside the brain totrigger this collapse?
SPEAKER_00 (00:59):
Aaron Powell At its core, it's a tragedy of
communication failure within thebrain.
The very first function that'salmost always affected is
short-term memory.
SPEAKER_01 (01:08):
Aaron Powell That mental filing system you use
every minute.
SPEAKER_00 (01:10):
Aaron Ross Powell Exactly that.
The one that lets you recallwhat you just heard or where you
put your keys a second ago.
As that starts to erode, it umit gradually impairs other
intellectual abilities.
SPEAKER_01 (01:22):
Aaron Powell So things like language, problem
solving.
SPEAKER_00 (01:24):
Trevor Burrus Yes.
And eventually it leads toseverely impaired judgment.
SPEAKER_01 (01:28):
Aaron Powell So we know the result is this
intellectual failure, but let'sdig into the biology.
What's the cause of thissystem-wide failure?
The sources seem to point toboth a physical and a chemical
breakdown.
SPEAKER_00 (01:38):
Aaron Powell Absolutely.
SPEAKER_01 (01:39):
Yeah.
SPEAKER_00 (01:40):
And what makes AD such a well such a challenging
puzzle is that we don't have onesingle undisputed trigger.
What researchers haveidentified, though, are two
primary culprits.
Two proteins?
Two proteins that startaccumulating in, frankly, toxic
amounts.
They essentially begin tosuffocate the brain's
communication network.
SPEAKER_01 (01:59):
Aaron Powell Okay, and this is where we need to
give you the specificvocabulary.
It's not just two proteins, isit?
SPEAKER_00 (02:03):
Correct.
So the first protein is calledamyloid beta.
When it builds up too much, itforms these dense, sticky
clusters outside the braincells.
SPEAKER_01 (02:12):
And these are the famous plaques?
SPEAKER_00 (02:13):
These are the plaques.
You can think of them like, Idon't know, massive road
construction that justcompletely jams up all the
neural traffic.
SPEAKER_01 (02:19):
Okay, that's a clear image.
And the second protein.
SPEAKER_00 (02:21):
The second is tau.
And this one is different.
It starts twisting into theseabnormal fibers inside the brain
cells, and that forms what wecall neurofibrillary tangles.
SPEAKER_01 (02:32):
So if the plaques are traffic jam outside the
cell.
SPEAKER_00 (02:36):
Then the tangles are internal structural damage.
It's like the support beams ofthe cell twisting and buckling
until the whole structure justcollapses from within.
SPEAKER_01 (02:44):
Wow.
So it's a physical traffic jamoutside and a structural failure
inside.
That's devastating.
SPEAKER_00 (02:50):
That's the physical component, yes.
But we also see a chemicalproblem.
Our sources r really emphasizethe role of acetylcholine.
SPEAKER_01 (02:58):
Which is a neurotransmitter.
SPEAKER_00 (03:00):
A critical one.
It's basically the chemicalmessaging service between brain
cells.
In patients with AD,acetylcholine levels just
plummet, which makes thecommunication failure from the
plaques entangles even worse.
SPEAKER_01 (03:11):
Aaron Powell So you have a physical block and a
chemical shortage.
SPEAKER_00 (03:14):
Exactly.
And the um the end result ofthat double whammy is that the
brain cells themselves start toshrivel and eventually they die.
SPEAKER_01 (03:22):
Aaron Powell Before we track how this looks from the
outside, the symptoms, let'sjust quickly touch on who is
most susceptible.
What does the research say aboutrisk factors?
SPEAKER_00 (03:31):
Aaron Ross Powell The risk factors are uh pretty
crucial for understanding thewhole landscape.
The biggest one, notsurprisingly, is simply
increasing age.
The risk just climbsdramatically after 65.
SPEAKER_01 (03:42):
And there's a family connection?
SPEAKER_00 (03:44):
Strong one.
Having a parent or a siblingwith AD significantly raises
your personal risk.
And then finally, there arecertain specific genetic factors
you can inherit that just makeyou more vulnerable.
SPEAKER_01 (03:53):
Okay, so let's connect that internal biology to
the outward experience.
AD is progressive.
The symptoms follow this, well,this distinct and often
heartbreaking timeline.
How do the sources break downthe stages?
SPEAKER_00 (04:05):
We can draw a pretty clear line between the early
stages, where a person can stillbe surprisingly independent, and
the later, more debilitatingstages.
SPEAKER_01 (04:14):
So what does that early phase look like?
SPEAKER_00 (04:17):
In the earliest phase, the challenges are almost
all focused on acquiring newmemories and trying to retain
new information.
SPEAKER_01 (04:24):
So they might repeat stories or forget a conversation
they just had?
SPEAKER_00 (04:29):
Precisely.
Or struggle to learn a newrecipe, something like that.
SPEAKER_01 (04:32):
So if they're forgetting what they had for
breakfast, that's early stage.
But they can still, say, buttontheir own shirt.
SPEAKER_00 (04:38):
That is the crucial nuance right there.
A person in early AD usuallyretains their ability to manage
their daily physical needs.
They can feed themselves, bathe,dress, groom, all without
assistance.
SPEAKER_01 (04:51):
The operating system is failing, but the hardware,
the motor functions, they'restill working.
SPEAKER_00 (04:56):
A great way to put it.
The basic self-care is stillintact.
SPEAKER_01 (04:59):
So when does that change?
When does the deterioration moveinto those middle and later
stages?
SPEAKER_00 (05:03):
Aaron Powell That's when the brain's executive
functions really begin tocollapse.
The loss shifts from just newmemories to the gradual erasure
of older, more distant memories.
SPEAKER_01 (05:13):
And this is where complex tasks become impossible.
SPEAKER_00 (05:16):
Exactly.
Things that require planning insequence: managing a budget,
preparing a meal with multiplesteps, or just remembering the
sequence of taking dailymedication.
SPEAKER_01 (05:26):
And I know a big one for caregivers is the loss of
spatial awareness.
SPEAKER_00 (05:30):
It is a huge source of anxiety.
The sources highlight the dangerof losing your sense of
direction, even in a placethat's completely familiar, like
your own neighborhood.
SPEAKER_01 (05:39):
Or even your own house.
SPEAKER_00 (05:40):
Yes, it's a profound loss of that internal map we all
have.
SPEAKER_01 (05:43):
And beyond memory and function, the psychological
and behavioral changes seem, Imean, they seem just as
devastating.
SPEAKER_00 (05:50):
They often are for everyone involved.
We frequently see personalitychanges, um, things like
irritability, escalatinganxiety, or really profound
depression in the earlierphases.
SPEAKER_01 (06:01):
But it gets more severe.
SPEAKER_00 (06:02):
It does.
As the disease moves into themiddle and late stages, these
symptoms can escalate prettyseverely.
SPEAKER_01 (06:08):
We're talking about delusions and hallucinations
here.
That must be incrediblydifficult to manage.
SPEAKER_00 (06:13):
Incredibly.
Delusions are these irrationalbeliefs.
A patient might sincerelybelieve someone is stealing from
them or that they're beingpersecuted.
Hallucinations are sensoryexperiences that just aren't
real seeing or hearing things.
SPEAKER_01 (06:27):
And this can lead to things like aggression.
SPEAKER_00 (06:30):
It can, and it's often combined with a very
dangerous tendency to wanderaway from home.
It just requires immense,constant protective care.
SPEAKER_01 (06:38):
Aaron Ross Powell That thought, that level of
cognitive distress really bringshome how difficult this
diagnosis must be, which iswhere we should go now.
Let's unpack this.
The affected person oftendoesn't recognize there's a
problem, right?
They might even deny it.
SPEAKER_00 (06:51):
It's very common, yes.
SPEAKER_01 (06:52):
So how is a diagnosis of AD actually
reached?
It must rely so heavily onfamily and friends.
SPEAKER_00 (06:58):
It absolutely does.
The diagnosis really relies onthe history gathered from the
people who see the person everyday, the ones who can report on
memory lapses, poor judgment, orpersonality changes.
The family is the cornerstone.
SPEAKER_01 (07:10):
And the big challenge, which are sources
stress, is that there is nosingle definitive test for
Alzheimer's.
You can't just get a blood testthat gives you a yes or no.
SPEAKER_00 (07:18):
That is correct.
The diagnosis is clinical.
It's built on, well, onexclusion and compiled evidence.
A doctor will start with amedical history, a physical and
neurological exam, and what'scalled a mental status exam.
SPEAKER_01 (07:31):
Simple cognitive tests.
SPEAKER_00 (07:33):
Right.
Simple tests involving visualtasks, writing, and memory
checks.
SPEAKER_01 (07:37):
Aaron Powell But, and this feels like the most
critical part of this sectionfor anyone listening.
Before a doctor even considersan irreversible diagnosis of AD,
they have to rule out otherconditions that can look just
like it.
SPEAKER_00 (07:48):
This step is profoundly important.
It is, frankly, the only chancefor a truly treatable,
reversible diagnosis.
SPEAKER_01 (07:55):
Aaron Powell And what's fascinating is that the
sources pinpoint two specificconditions that can perfectly
mimic AD symptoms.
SPEAKER_00 (08:01):
They can.
And if they're caught, theoutcome is completely different.
We're talking about very lowlevels of vitamin B12 or a very
underactive thyroid, also knownas hypothyroidism.
SPEAKER_01 (08:10):
Wait, so a vitamin deficiency or a thyroid issue
can cause cognitive declinesevere enough that it looks like
Alzheimer's?
SPEAKER_00 (08:17):
That is precisely the danger and also the hope.
The incredibly importanttakeaway for you is that the
memory and thinking problemsfrom these issues can improve
and even go away entirely withtreatment.
SPEAKER_01 (08:29):
Wow.
So if a doctor skips that step,those simple blood tests.
SPEAKER_00 (08:32):
They might unnecessarily doom a patient to
an irreversible diagnosis whenthe real problem is entirely
fixable.
SPEAKER_01 (08:39):
That makes the blood work just about the most
important tool in the wholeprocess.
It's like checking the oilbefore you declare the engine is
broken for good.
SPEAKER_00 (08:46):
A perfect analogy.
So if those simple tests comeback clean, but cognitive
problems are still there, what'snext?
SPEAKER_01 (08:53):
Right.
What's the next step?
SPEAKER_00 (08:55):
They might move on to more detailed
neuropsychological testing,which is a much deeper dive into
cognition, and they'll almostcertainly order brain imaging
studies, a CT scan or an MRI.
SPEAKER_01 (09:05):
But it's vital to understand what these scans can
and maybe more importantly,cannot do.
SPEAKER_00 (09:10):
Yes.
They cannot diagnose AD withcertainty.
SPEAKER_01 (09:13):
But they rule other things out.
SPEAKER_00 (09:14):
Exactly.
They are critical for ruling outother structural causes, things
like a brain tumor or evidenceof a stroke.
The scans can show brainshrinkage or atrophy, which
supports a clinical diagnosis ofAD, but it's still not
definitive proof.
SPEAKER_01 (09:29):
And the diagnosis is usually confirmed by a
specialist.
SPEAKER_00 (09:32):
Yes, after referral to a neurologist, a
geriatrician, or maybe ageriatric psychiatrist.
SPEAKER_01 (09:38):
Aaron Powell So the picture is clear.
AD is irreversible.
Function declines until death.
The goal has to shift entirelyto management.
What do the sources say aboutproviding some hope, both in
delaying the onset and slowingit down once it starts?
SPEAKER_00 (09:51):
Let's start with prevention, or maybe more
accurately, delaying the onsetof symptoms.
The evidence we have stronglysupports simple lifestyle
factors that you can controlright now.
SPEAKER_01 (10:01):
Like staying active.
SPEAKER_00 (10:03):
Staying physically and mentally active is key.
Regular physical exercise,particularly aerobic exercise,
seems to be very protective.
SPEAKER_01 (10:10):
And diet always comes up in these conversations.
SPEAKER_00 (10:12):
He does.
The sources specificallyhighlight a dietary pattern,
kind of like a Mediterraneanstyle.
They emphasize a diet withplenty of fish, olive oil, and
lots of vegetables.
SPEAKER_01 (10:21):
So this is about delaying onset and maybe slowing
progression.
SPEAKER_00 (10:25):
It seems to be, yes.
It just underscores that what'sgood for your heart and your
vascular health is also reallygood for your brain.
SPEAKER_01 (10:31):
Okay, let's shift to treatment for those already
diagnosed.
What are the workhorse drugsthat aim to slow the decline?
SPEAKER_00 (10:38):
For mild to moderate AD, we rely on a class of drugs
called cholinesteraseinhibitors.
Now, since we saidacetylcholine, the brain's
messenger, is in short supply.
SPEAKER_01 (10:48):
Right.
SPEAKER_00 (10:49):
These drugs work by inhibiting the enzyme that
breaks it down.
SPEAKER_01 (10:52):
So you're basically preserving what little of the
messenger chemical is left.
SPEAKER_00 (10:55):
That's a great way to think about it.
You're helping the brain makethe most of its existing supply.
For moderate to severe AD,there's also a drug called
mementine, which works a bitdifferently to help stabilize
memory.
SPEAKER_01 (11:07):
And now we have to talk about the newer, more
complex therapies, the ones thathave been all over the news.
This is where we need to becautiously optimistic.
The monoclonal antibodies.
SPEAKER_00 (11:18):
We are.
We're talking specifically aboutaducanimab, aduhelm, and the
newer one, Lacanimab, um,Gipsula.
Both got accelerated FDAapproval.
SPEAKER_01 (11:27):
And unlike the other drugs that just manage symptoms,
these are designed to attack theunderlying problem.
SPEAKER_00 (11:33):
Exactly.
They target and try to clear outthose amyloid beta protein
deposits we talked aboutearlier, the plaques.
SPEAKER_01 (11:39):
The hope being if you clear the plaques, you might
slow or even halt the disease'sprogression.
But the sources are very clearthat we have to stress the
caution around these drugs.
SPEAKER_00 (11:50):
We absolutely must.
While they represent a huge leapforward in targeting the disease
mechanism itself, they come withsignificant risks.
The main concern is somethingcalled amylaid-related imaging
abnormalities or ARAA.
SPEAKER_01 (12:03):
ARAA, and what is that?
SPEAKER_00 (12:05):
It refers to side effects you can see on brain
scans, specifically brainswelling or microhemorrhages,
tiny little bleeds in the brain.
SPEAKER_01 (12:12):
That sounds extremely serious.
SPEAKER_00 (12:13):
It is.
Patients on these drugs have tobe monitored with regular MRI
scans to catch these thingsearly.
It really turns the treatmentdecision into a very careful
risk versus reward calculation.
SPEAKER_01 (12:24):
So beyond the pharmaceuticals, supportive
non-drug care is stillabsolutely essential.
SPEAKER_00 (12:29):
It's paramount.
The supportive environment iseverything.
Caregivers need to maintainfamiliar surroundings, people,
and routines.
Too much change can triggerconfusion and agitation.
SPEAKER_01 (12:40):
And creating safe environments to manage things
like laundering.
SPEAKER_00 (12:43):
Critical.
And also making sure the patientstays engaged, even as their
abilities fade.
SPEAKER_01 (12:48):
Through things like music or art therapy.
SPEAKER_00 (12:51):
Precisely.
Music, art, occupationaltherapy.
They all provide essentialstimulation and can offer real
emotional outlets.
It really takes a whole team.
SPEAKER_01 (12:59):
This deep dive has really given us a much clearer
picture of AD from the biologyof plaques and tangles all the
way to the cutting edge of thesenew, if controversial,
therapies.
SPEAKER_00 (13:08):
I hope so.
SPEAKER_01 (13:09):
And I think most importantly, we've highlighted
that critical need for a properdiagnosis, making sure to rule
out treatable conditions like aB12 deficiency or thyroid issues
before accepting thatirreversible diagnosis.
SPEAKER_00 (13:21):
Alzheimer's remains a severe challenge, there's no
doubt.
But this kind of informedapproach, combining lifestyle
efforts, early and comprehensivediagnosis, and the uh the
careful use of moderntreatments, that offers the most
critical path forward.
SPEAKER_01 (13:35):
And that leaves us with a final provocative thought
for you to consider as youreflect on all this.
If optimized lifestyle choices,physical and mental activity,
diet, and exercise, arescientifically shown to delay
the onset of symptoms and slowdisease progression later in
life, how much earlier in lifedoes the compounding biological
benefit of an optimizedlifestyle truly begin?
(13:56):
Something for you to mull overuntil our next deep dive.
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