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June 1, 2025 35 mins

Listen in as our expert panel discusses medications for the treatment of Alzheimer dementia.  They'll review the risks and benefits of cholinesterase inhibitors, memantine, and the anti-amyloid monoclonal antibodies.  And you’ll hear strategies for managing behavioral and psychological symptoms of dementia.   

Special guests:

  • Tatyana Gurvich, PharmD, BCGP, APh
    • Associate Professor of Clinical Pharmacy
    • Mann USC School of Pharmacy
    • UCI Senior Health Center
  • Candace Pierce, DNP, RN, CNE, COI
    • Nurse Educator, Nurse Planner, and Healthcare Leader
    • Colibri Healthcare
  • Darlene Moyer, MD, FAAFP
    • Associate Director, HonorHealth Family Medicine Residency Program
    • Associate Professor of Clinical Practice – SOMME – Arizona State University
    • Clinical Associate Professor – University of Arizona College of Medicine - Phoenix

You’ll also hear practical advice from panelists on TRC’s Editorial Advisory Board:

  • Stephen Carek, MD, CAQSM, DipABLM
    • Clinical Associate Professor of Family Medicine
    • Prisma Health/USC-SOMG Family Medicine Residency Program
    • USC School of Medicine Greenville
  • Craig D. Williams, PharmD, FNLA, BCPS
    • Clinical Professor of Pharmacy Practice
    • Oregon Health and Science University

None of the speakers have anything to disclose. 

This podcast is an excerpt from one of TRC’s monthly live CE webinars, the full webinar originally aired in April 2025.

TRC Healthcare offers CE credit for this podcast. Log in to your Pharmacist’s Letter, Pharmacy Technician’s Letter,or Prescriber Insights account and look for the title of this podcast in the list of available CE courses.

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Transcript

Episode Transcript

Available transcripts are automatically generated. Complete accuracy is not guaranteed.
(00:01):
This transcript is automatically generated.

Darlene Moyer (00:07):
I really love this topic because I think it's
an opportunity to really grabpeople's attention about the
importance of these healthylifestyle factors.
And people pay attention whenyou start talking about dementia
because dementia really scarespeople.
Most people have had contactwith somebody with advanced
dementia and worry about gettingthat themselves.

(00:29):
And I think it's a really goodopportunity to stress these
basic things that people can doto really minimize their risk.

Narrator (00:37):
Welcome to Medication Talk, an official podcast of TRC
Healthcare, home ofPharmacist's Letter, Prescriber
Insights, and the most trustedclinical resources.
Proud to be celebrating 40years of unbiased evidence and
recommendations.
On today's episode, listen inas our expert panel discusses

(00:57):
medications for the treatment ofAlzheimer's dementia.
They'll review the risks andbenefits of cholinesterase
inhibitors, memantine, and theanti-amyloid and monoclonal
antibodies.
And you'll hear strategies formanaging behavioral and
psychological symptoms ofdementia.
We have several excitingspecial guests on this episode,
including Dr.

(01:17):
Tatyana Gurvich, AssociateProfessor at the USC Mann School
of Pharmacy, Dr.
Candice Pierce, CourseDevelopment Manager and Nurse
Planner at Elite Learning, andDr.
Darlene Moyer, AssociateDirector of Honor Health Family
Medicine Residency Program andClinical Associate Professor of
Family Medicine and GeriatricMedicine at the University of
Arizona College of Medicine.

(01:37):
You'll also hear practicaladvice from panelists on TRC's
Editorial Advisory Board, Dr.
Stephen Carrick from the USCSchool of Medicine, Greenville,
and Dr.
Craig Williams from the OregonHealth and Science University.
This podcast is an excerpt fromone of TRC's monthly live CE
webinars.
Each month, experts andfrontline providers discuss and

(01:58):
debate challenges in practice,evidence-based practice
recommendations, and othertopics relevant to our
subscribers.

CE Narrator (02:05):
And now, the CE information.

Narrator (02:10):
This podcast offers continuing education credit for
pharmacists, pharmacytechnicians, physicians, and
nurses.
Please log in to yourPharmacist's Letter, Pharmacy
Technician's Letter, orPrescriber Insights account and
look for the title of thispodcast in the list of available
CE courses.
None of the speakers haveanything to disclose.
Now let's join TRC editor Dr.

(02:32):
Sara Klockars and start ourdiscussion.

Sara Klockars (02:34):
So Craig, we'd like for you to jump in and
share with us what some of thebrain changes are that occur in
Alzheimer's disease so we cantalk about the medications and
where they might work down theroad.

Craig Williams (02:52):
Yeah, no, it's a good question.
Obviously, in appliedpharmacology, the goal is always
to understand the physiologyand then develop therapies that
directly treat the physiology.
And it's been challenging inAlzheimer's dementia.
So the two major kind ofchanges that we know about in
the brain structure and has beenidentified now for a couple of
decades are the increasing inamyloid beta plaques and then

(03:15):
increasing in these tau proteintangles.
And There's just a nice paperabout a year ago out of a group
in China that's doing alongitudinal following of older
adults in that country andactually doing some intermittent
sampling of cerebral spinalfluid and kind of looking for
when changes occur and how theyprogress.
And so they've kind of nicelyshown that these start well over

(03:36):
two decades before any kind ofdetectable cognitive changes
with maybe amyloid beta changespreceding tau.
It's kind of unknown.
But unfortunately, while thecorrelation is strong, the The
causation is still hard toprove, but those are two
structural changes.
The other aspect mentionedthere is known changes in
neurotransmitter concentrations,the way neurotransmitters

(03:57):
behave in these patients'brains, and whether or not any
of those are directly related tothe kind of physical changes
mentioned is also not realclear.
But there's definitelydecreased signaling via
acetylcholine, and that plays afundamental role in all kinds of
signaling in the brain.
And then a relative excess ofexcitatory signals transmission,
so mostly through glutamate, asnoted there.

(04:19):
So it's still a not realunderstood imbalance.
But as we'll get a chance todiscuss, medications have been
marginally successful inaddressing those changes.
The neurotransmitter changeshave been less successful in
trying to address the physicalchanges to slow the progression
of the disease.

Sara Klockars (04:36):
Thank you for that.
And you had mentioned some ofthose changes you know, happen
decades before we start to seeany symptoms.
So Tatyana, could you reviewthe progression of Alzheimer's
disease for us?

Tatyana Gurvich (04:51):
Sure.
So it is truly a progression.
You start with preclinicalphase, which is basically no
symptoms that anybody cannotice.
And that transitions to mildcognitive impairment.
This stage can last up to fiveyears, and sometimes it
progresses to dementia, andsometimes it doesn't.
Generally speaking, patientshave mild symptoms.

(05:14):
They may have very mild changesin memory, or symptoms will be
amnestic in nature.
Sometimes there's slightchanges in executive
dysfunction, so more issues withplanning things.
And with more substantialtesting, neuropsych testing, you
can actually pick up mildcognitive impairment a lot more

(05:34):
frequently than with sort oftraditional kind of screening
tools that we have.
So after mild cognitiveimpairment, sometimes the
disease progresses into variousstages of dementia.
So that will be mild dementia,moderate dementia, and severe
dementia.
And with mild dementia, youbegin to see problems with some

(05:56):
daily activities and they kindof progress as you go from mild,
moderate to severe.
In the mild cognitiveimpairment stage, there is
evidence of pathology.
So you do notice the biomarkerslike the beta amyloid plaques
and the tau protein and that'swhy some of these monoclonal
antibodies that just came outare effective, were more

(06:18):
effective in the earlier stageslike mild cognitive impairment
and mild dementia.

Sara Klockars (06:22):
Thanks for that background.
Craig, could you give us ahigh-level overview of the meds
that impact cognition and memoryand how they work?
And then we'll get to behaviorsin a bit.

Craig Williams (06:37):
We have had some modest success in addressing
the current neurotransmitterchanges.
So the cholinesteraseinhibitors is probably most
commonly known to most listenersand readers of donepezil.
These can inhibit the enzymethat breaks down acetylcholine.
Acetylcholine, again, playsthat complex role in central
neurotransmission, but does seemto help focus and help

(06:59):
cognition a bit.
So restoring some cholinergicfunction to the cerebral cortex
and the brain.
And those, again, we'll talk abit more about how effective
they are and kind of where weuse them in therapy, but
directly increasingacetylcholine function.
As disease progresses, andmemantine 's
been around now for just overtwo decades, but it's an NMDA

(07:22):
blocker.
NMDA is one of the receptorsfor glutamate, that stimulatory
neurotransmitter.
So idea there being it's amodest blocker.
So we have more potent blockersof NMDA that have untoward
effects.
But in this case, we're usingkind of a modest blocker to
presumably take the foot off theaccelerator a bit to the

(07:44):
overactive neurotransmitter.
So again, not real well workedout how the physiology in the
brain kind of corresponds toimprovements in symptoms.
But so we can increase the lackof acetylcholine and we can
somewhat damp down the excessglutamate with the two major
classes we have with the Thankyou.

(08:04):
Thank you.

Sara Klockars (08:28):
Darlene, would you want to comment just on how
the anti-amyloid monoclonalantibodies are thought to work?

Darlene Moyer (08:36):
So, you know, the idea is that your immune system
is trying to go in and clearout the amyloid plaques.
And that, as Craig was saying,really leads to the risks of the
medication as well, because Iknow we'll talk about this down
the line some, but the biggestrisk is that anytime you're
creating this inflammatoryresponse and attacking something

(08:56):
in sensitive tissue, you canthen start to have some damage
and some bleeding and someedema, which is what leads to
the side effects that we'reseeing on the MRI change.
and having some bleeding in thebrain, which is obviously never
a good thing.

Sara Klockars (09:10):
Thank you for that high-level overview of the
meds we have available fortreating cognitive symptoms of
Alzheimer dementia.
So let's move along and talkabout the role of the meds, dig
into some specifics, and thenanswer some questions from our
listeners.
And so, Tatyana, I was hopingyou could review with us some of

(09:30):
the common meds that we shouldbe avoiding in patients with
dementia.

Tatyana Gurvich (09:37):
Those are all of your anticholinergic meds.
So anything with any kind ofanticholinergic profile, your
old tricyclic antidepressants,for example, some of the
atypical antipsychotics likeolanzapine, a bunch of OTC drugs
like diphenhydramine,doxylamine, other antihistamines

(10:00):
like hydroxyzine that we oftenuse for itching and some
psychiatrists use it foranxiety, things like urine
antispasmodics, the worst onebeing oxybutynin, but also some
of the newer ones also likeVesicare and Enablex, Detrol,
even those have significantanticholinergic profile.
GI antispasmodics that we woulduse in our patients with like

(10:25):
IBS, for example, with apredominant symptom of diarrhea,
all of those medications haveanticholinergic profile.
Something like Lomotil that wewould use for diarrhea has
atropine in it, which isanticholinergic muscle relaxants
like cyclobenzaprine actuallyare relative of a tricyclic
antidepressant structurally.
Paroxetine, which is a SSRI,and we don't think of SSRIs as

(10:49):
having anticholinergic burden,but paroxetine does.
Some of the other things thatcan contribute to confusion and
cognitive impairment are thingslike benzodiazepines.
Certainly can cause confusionand cognitive slippage.
Things like the Z drugs,Ambien, Lunesta, Sonata are also
on the list.
And then you have to look atthings like cocktails, CNS

(11:11):
active cocktails.
When they're taking a bunch ofdifferent drugs that affect the
CNS, are they going to haveslower speed of processing?
Is that going to impaircognitive function in those
patients?
And then you have to look atalcohol and cannabis.
I mean, in my patientpopulation, there are all kinds
of older adults who want to usecannabis for all kinds of
reasons.

(11:31):
But at this point, I don't knowthat there's that much research
in the frail older patients andthe use of cannabis.
We've seen a number of cases ofpatients coming in with
significant cannabis use andcognitive impairment as well.
And of course, alcohol.
The amount of alcohol an olderadult can drink safely is
significantly less than it waswhen they were younger, for

(11:54):
example.
So all those things have to belooked at as reversible causes.
And these are super easy to getrid of.
And hopefully, your mind clearsup a little bit

Sara Klockars (12:06):
Excellent.
And we can help find saferalternatives.
Would you want to comment onconsideration?
So how do you decide whichmedication to choose?

Tatyana Gurvich (12:16):
Sure.
So typically for mild dementia,mild to moderate dementia, you
would first start probably acholinesterase inhibitor.
Which of the cholinesteraseinhibitors you start, I don't
know that it makes a whole lotof difference.
In my practice, we use a lot ofdonepezil.

(12:36):
It's relatively easy toadminister.
It's a single pill once a day.
You start with five milligrams.
You wait at least four weeks,sometimes longer, and you go up
to 10 to maximize benefit, andyou monitor for side effects.
So the biggest issue with thecholinesterase inhibitor are its
side effects.
So you can get thesecholinergic kinds of symptoms

(13:00):
like diarrhea, urinaryfrequency.
And if you're dealing with anolder, frail adult, that could
easily translate into urinaryincontinence.
And that's a huge life-stoppingkind of an event, right?
You want to make sure they'renot having a significant
bradycardia.
So a pulse in the 50s isprobably okay, but less than

(13:22):
that is probably problematic.
You're also looking for anexacerbation of agitation or
worsening of symptoms when youfirst start the medication.
So you're looking at all ofthat.
And if the patient toleratesit, okay, you can go from 5 to
10 milligrams pretty easily.
Donepezil also comes in ahigher strength dose of 23 in

(13:43):
our experience.
In my clinic, at least, wenever use it.
I think the higher dose justtranslates into more cholinergic
side effects, which patientscan't always tolerate.
The other thing you're lookingfor with a cholinesterase
inhibitor is because it'scholinergic, you're going to get
watery eyes, runny nose, thosekinds of symptoms, drooling
sometimes.
And so patients have runnynose, watery eyes.

(14:06):
They think they have allergies.
So they run to the pharmacy andbuy a diphenhydramine or a
chlorpheniramine or abrompheniramine, some kind of
an old-style antihistamine,which can actually cause the
opposite problem.
It can cause cognitiveslippage.
So you want to make surethey're not doing that.
For more advanced dementia, somoderate to severe dementia, you

(14:27):
might introduce memantine,which is an MDA receptor
blocker.
You can use it in combinationwith cholinesterase inhibitors
or by itself in more severedisease.
I think they're bettertolerated.
than cholinesterase inhibitorsin general, the biggest issue
you're looking for is anincrease in agitation when you

(14:48):
start the medication.
But if that doesn't happen,overall, they're tolerated
pretty well.
Some people will get a littlediarrhea.
Some people will get insomnia.
Some people will get a littledizziness, headaches.
But most of the time, they'retolerated fine.
So some of your more advanceddementia patients will be on
both cholinesterase inhibitorsand memantine.
In terms of Dosing formulationslike donepezil comes in a

(15:12):
patch.
Is there a benefit to that?
Probably from a compliancestandpoint, maybe.
But in terms of coverage,insurance coverage?
I don't know of a Medicare PartD plan that will cover a patch.
Rivastigmine is anothercholinesterase inhibitor that we
sometimes use.
It comes as pills and patches.
I think the reason theydeveloped a patch is because in

(15:34):
oral form, they were so poorlytolerated and had so many
cholinergic kinds of sideeffects that the only way you
can tolerate rivastigmine iswith a patch.
So sometimes we use that ifpatients have trouble swallowing
or don't like to take pills.
But those are the two that wemostly use donepezil, 5 to 10
milligrams, or rivastigmine,usually in patch form, and then

(15:57):
a combination of them for moreadvanced disease and usually
cholinesterase inhibitors formilder symptoms.

Sara Klockars (16:05):
Thank you for that.
Darlene, what do you mostcommonly use in practice?

Darlene Moyer (16:11):
I think that was a great summary.
I most commonly use donepezilas well, just because it's most
available, it's fairlyinexpensive, and it's the one,
you know, frankly, that we'remost familiar with.
And I think I start to move topatch form of rivastigmine if
somebody's having, you know, alot of GI upset with donepezil,

(16:32):
or if just from a compliancestandpoint or, you know, ability
to swallow medications, theyneed to be up on a patch for
those reasons.

Sara Klockars (16:40):
And I know there was recently a new prescription
approved, Benz- galantamine.
Do you see that as having arole?
I

Tatyana Gurvich (16:49):
saw galantamine used when it first came out
when I was actually in a familypractice residency program.
Some neurologists wereprescribing it, and we would get
patients on them.
But since I've been in mygeriatrics practice, we don't
have a single patient ongalantamine, and certainly not
on that new one.
With Medicare Part D coverage,issues, especially this year, I

(17:12):
cannot imagine that it's goingto be covered at all, and
certainly not anytime soon.
I don't know what everybodyelse thinks.

Darlene Moyer (17:22):
I'll be honest, I haven't used this at all.
And, you know, when I looked itup to review it, I understand
it's only twice a day dosing aswell, which just from a ease of
administration standpoint isreally difficult for patients.

Sara Klockars (17:37):
Thank you.
And so when starting thesemedications, we kind of talked
about some of the considerationsand side effects and risks.
Can you share a conversationthat you have had with a patient
or a caregiver regarding thebenefits of these medications
and the realistic expectationsthat they can see in their

(17:58):
day-to-day life?

Tatyana Gurvich (18:01):
So The conversation I have with my
patients is that whether you'restarting donepezil or memantine,
what these drugs generally dois delay the progression of
symptoms and delay theprogression of the dementia.
So a lot of the times when youstart these medications, you

(18:21):
really, if you notice no change,that for a long period of time,
that probably means the drug isworking.
I think if they're expecting tosee an improvement in cognition
or daily activities, I thinkthat may be an unrealistic
expectation.
So most of the time, you kindof see no change and you're

(18:43):
stable at the level you wereprior to starting the
medication.
I do go over all the sideeffects and making sure that
they know how to deal with themand if they develop side effects
that they just can't manage andlike incontinence being one of
them to come back and we cantalk about options.
Sometimes they're on a higherdose of donepezil, you back off

(19:05):
a little bit to the lower doseto see if that improves things.
Sometimes you add memantine alittle bit earlier, that
happens.
Family members, patients,caregivers have to realize the
limitations of these drugs, thatthey're not going to
necessarily makethe patient better, they may probably just keep them at the level they're at, longer.

Sara Klockars (19:27):
Does anyone else want to chime in about common
misconceptions some of yourpatients have had about these
medications?

(19:54):
I agree that expectation management in the conversations is probably most important and I always try to take time to make sure that family members before we even really talk about medications, make sure that they understand that dementia is a progressive disease and that it is going to move forward the pace at which it's going to move forward is variable between patients, but especially with Alzheimer's, there's a very clear progression of symptoms. I usually will take the fast scale for dementia, which is essentially a scale that correlates symptoms with stage of disease, and I'll even give copies of that to patient families so that they can kind of see what's coming next. And I think once they understand thatpart, it makes it easier to

(20:20):
have the conversation aboutmedication expectations, because
sometimes pausing thosesymptoms, like Tatiana was
saying, or even if you can atvery best turn the clock back by
about six months or so, thatmight be a great thing.
And that might actually buypatients and families time when
they're trying to make decisionsabout needing to look into

(20:41):
other living situations, lookinginto assisted living or memory
care centers.
Even a little bit of extra timemight be helpful, but But I
always make sure that theyclearly understand that this is
still going to be a progressivedisease, whether or not we use
the medications.

Candace Pierce (20:58):
I absolutely agree that education is so
important.
When we first start havingthese conversations with
families, This is a time that itis very hard for them to really
latch on and understand whatyou're saying because they're
just trying to digest the factthat they've received this
diagnosis and their whole worldis about to change and all their
roles are about to shift.
And so I find that having theseconversations, just little

(21:21):
reminders as they're coming infor appointments and is really
good so that it's not sooverwhelming for the family.

Sara Klockars (21:30):
Thank you.
And another question we havehad from subscribers is, so if
patients are starting on theseanti-amyloid monoclonal
antibodies for early onset ormild cognitive impairment, can
we add cholinesterase inhibitorsor memantine to those

(21:51):
antibodies?

Darlene Moyer (21:53):
Yes, you can.
Most of the patients right nowthat are getting these
monoclonal antibodies are partof a trial or are at a big
research center.
So if you're going to be theone outside of that center
making changes to theirmedications, you would always
want to communicate with theteam that was overseeing the
protocol that they were enrolledwith.
But yes, you can use them.

(22:15):
And actually, most of thestudies are being done in
patients who are already onmedications for dementia as
well.

Sara Klockars (22:22):
Thank you.
And then another questionthat's come up is, when do you
consider stopping medicationsfor dementia?
And are there risks withstopping these medications?
So how do you approachdeprescribing with the patient
and caregiver?

Tatyana Gurvich (22:39):
So some of the reasons to discontinue would be
if they're non-adherent, ifthey're not taking it on a
regular basis, if there'scontinued deterioration despite
being on medications, if there'ssudden increase in
comorbidities and it just makesit more difficult to manage
another medication, or ifthere's drug interactions that

(23:01):
occur with the current regimen.
And also, you want to getpatient input, if possible,
caregiver input, family input.
Sometimes it's their decisionto decide to stop.
I think if the patient isstable and is not experiencing a
decline, I think it's worth itto continue because sometimes

(23:22):
what we do see is when you stopa medication and they do kind of
regress a little bit morequickly, and then when you
restart the med, it's hard tobring it back up to that level.
I think that would be the onlyrisk of stopping the medicine,
that a patient couldsignificantly decline shortly
after the But if there is adecline in function and

(23:43):
cognition anyway, and it becomesmore cumbersome to take the
medicine, then I think it isokay to discontinue it.

Sara Klockars (23:51):
And can patients just stop them, or do they need
to taper them?

Tatyana Gurvich (23:56):
They should be tapered over some time.
Usually, like if you're on anepisode 10, you should probably
go to 5 for about a month andthen see how you do, and then
you discontinue.
So they shouldn't be abruptlydiscontinued.

Craig Williams (24:10):
Yeah, if you're on anything but the starting
dose, then moving down is a goodidea.
So although to the earliercomment, often five of
donepezil is a dose patientsare on when we're seeing them.
So in which case there's nofurther tapering down to do.

Sara Klockars (24:23):
Thank you.
What are some of those dementiabehaviors that we may see and
non-drug measures to considerfor managing those?

Candace Pierce (24:35):
Your non-drug measures are really going to
focus on promoting physical andemotional comfort.
You have a lot of symptoms thatcome with dementia from
agitation and aggression, and alot of times We want to try to
make adjustments to ourenvironment to reduce that
aggression and agitation andconfusion that they're going
through.
And so that can be things assimple as minimizing noise,

(24:57):
getting rid of the clutter, evenadequate lighting.
If the lighting is too brightand just overstimulating, it
really overwhelms their senses.
So you really want to work oncreating a calm environment and
also structured routines foractivities like their eating,
their toileting, their sleeping,because that's going to create
that stability and also helpreduce some of that anxiety,

(25:19):
which is going to, of course,reduce agitation and aggression.
Some of the other things thatthey do as well as you can do,
we use the word therapy a lot.
So music therapy, whitetherapy, aromatherapy, things
that are calming and soothing tothem.
There's also cognitivestimulation that's really
important as well.

(25:40):
So having those structuredinteractions and those daily
routines, the goal there isreally just to try to preserve
the patient's abilities and evento help them draw out some of
their memories as long aspossible and making those
connections in their brains.
And a lot of the caregivers canbe trained and receive

(26:01):
education on how to interactwith their loved one through
these different types of, youknow, there's validation
therapy, reminiscent therapy toreally help with that.
So I do encourage a lot of thecaregivers to try to work on
creating these routines and, youknow, what are some of the
things that their loved oneenjoy doing and how can we put

(26:22):
that into their day?

Sara Klockars (26:25):
Stephen, did you have anything else to add, or do
you want to comment on someother meds you may see or use
for dementia-related behavioralor psychological symptoms?

Stephen Carek (26:37):
Yeah, I mean, primary, at least assistance is
with a lot of these non-drugtherapies, but we'll use some
other medications to hopefullyhelp address some of those
disruptive behaviors ortendencies that we're seeing
from our patients.
I think one thing is trying toaddress underlying pain.
I think it's one thing we tendto think about when we're
dealing with patients who may beconfused or behaviors may be

(27:01):
significantly deviating fromwhat their previous patterns may
be.
And we know that chronic painmay exacerbate some of these
dementia-oriented papers aswell.
I think it's one of the thingsthat the top of the list is
Tylenol and whether Tylenol canhelp with some of these dementia
behaviors in helping addressmaybe to calm down some of those
pain symptoms that patients mayhave.
There's also other medicationslike antidepressants for some

(27:22):
mood-related symptoms.
We also, I mean, all thesemedicines as we continue
forward.
antipsychotics,mood-stabilizing medicines,
approaching those patients andtrying to address what is the
hope with these medications andhelping either address or
augment the dementia medicationsthat we're utilizing, but also
weighing the side effects fromthem.
Because many of these listmedications are also on the

(27:43):
BEERS list.
Utilizing some of these,especially like antipsychotics,
may increase risk for mortality.
Really, really stronglyconsidering those risk and
benefits is really importantwhen trying to address some of
those other behaviors that arenot being controlled or managed
well with some of their dementiamedicines they may be currently
on.

Craig Williams (28:04):
Yeah, I'll just add, Sarah, briefly, we discuss
all the time that generally wehave lots of medications that
make dementia and cognitionworse and not a lot that make
them better.
So we've talked a lot abouttaking a holistic approach to
these medications, to patients'medication lists, looking for
things that may be exacerbatingadverse effects of therapies we
want to keep on board you canget rid of and But also just
recognizing that a lot of thingsget added by providers that may

(28:28):
not be taking care of thecognitive aspects of the patient
can worsen things.
So just being very alert tothat med list.
And yeah, so many things can,the whole list of medications
talked about, you try to avoidearly disease to just kind of
make it worse later on.

Tatyana Gurvich (28:44):
Can I just add to that?
So when you're talking abouttrying antipsychotics, like
People said there is this blackbox warning for increased risk
of mortality.
with them.
And so when you're talkingabout agitation, I think it's
really important to identifyspecific behaviors that patients
are experiencing.
Because, you know, agitation tome could mean one thing, to a

(29:07):
caregiver it could meansomething else, or really
agitation exhibited by.
And the behavior has to be adanger to the patient or a
danger to the caregiver.
If that's the case, thenantipsychotics at low doses may
be appropriate.
But you have to kind of hone inon that behavior.
And as you're titrating up thedose gradually to see if the

(29:28):
behavior goes away.
These drugs aren't effective inall patients.
And in fact, a lot of timesthey're ineffective.
And so you have to decide whento treat and how to treat and
kind of monitor the treatmentcarefully to make sure it's
effective and doesn't produceadverse events.

Craig Williams (29:47):
Yeah, it's a great reminder.
They're for the agitation.
They're not for the cognition.
So they They do not improvecognition, it's just for
agitation.
So yeah, it's a great pointthat what is agitating them and
can we do anything else tomitigate the need or less the
need for an antipsychoticknowing it's not going to help
the end-of-line disease process.

Sara Klockars (30:05):
So let's just transition really quick to
dementia risk reduction.
What are some strategies yourecommend or that have evidence
to support reducing the risk ofcognitive decline?

Stephen Carek (30:19):
I think some of the big risk factors that we
address, especially if we canaddress early in life, early
adulthood through middle age,healthy weight, really focusing
on things like regular physicalactivity, exercise, managing
those comorbidities of highblood pressure, diabetes,
limiting substances that mayaffect cognition, especially

(30:40):
with chronic and damaging uselike alcohol, tobacco cessation.
Other things that I really liketalking about too is sleep with
patients.
I think sleep is a huge, Ithink poor sleep and
dysfunctional sleep is also asignificant risk factor for
developing dementia later inlife.
So really trying to identifypatients who have sleep apnea,
intervene, but really helpingpatients develop good sleep

(31:00):
hygiene habits.
I know there's some theorybehind the glymphatic system and
being able to help reduce sortof the tau buildup that may
occur and cause dementia andsleep, and the glymphatic system
can be a huge process in that.
But encouraging just overallholistically healthy lifestyles,
promoting healthy behaviorslike healthy diet, healthy
exercise and physical activitypatterns, and reducing those

(31:21):
toxic or damaging substances,namely alcohol, tobacco,

Darlene Moyer (31:25):
I agree.
I really love this topicbecause I think it's an
opportunity to really grabpeople's attention about the
importance of these healthylifestyle factors.

(31:48):
And then the benefit is thatthese things also are all items
that help promote healthy aging,maintenance of physical
function over time, and all theother parts of aging that we
want to improve for people aswell.

Sara Klockars (32:12):
Thank you.
I have one last subscriberquestion.
So do GLP-1 agonists have arole in dementia?

Darlene Moyer (32:20):
I have not yet heard any definitive evidence
one way or the other.
I suspect over the next coupleof years we'll have lots of
studies and hopefully get somegood answers for this.
But so far, I haven't heard anycompelling evidence one way or
the other.

Stephen Carek (32:36):
The best theory I've had would be GLP-1s do so
much.
And I think there's a centraltheory of the inflammatory
reduction that occurs withGLP-1s may be driven by a lot of
the weight loss and especiallyleading to obesity being maybe
also a disease of chronicinflammation.
Through that, is there apossibility?
Maybe, yes.
But again, the evidence is notthere yet.

(32:56):
But there could be somepromising data that could help
support that.

Narrator (33:03):
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from listening into thisdiscussion.
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additional materials on thistopic, like charts and other
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If you're not yet apharmacist's letter, pharmacy
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