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.
The clinical resources mentioned during the podcast are part of a subscription to Pharmacist’s Letter, Pharmacy Technician’s Letter, and Prescriber Insights:
- FAQ – Alzheimer Dementia Pharmacotherapy
- Chart – Pharmacotherapy of Dementia Behaviors
- Chart – Drugs with Anticholinergic Activity
- Chart – Potentially Harmful Drugs: Beers Criteria
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Transcript:
Darlene Moyer:
I really love this topic because I think it’s an opportunity to really grab people’s attention about the importance of these healthy lifestyle factors. And people pay attention when you start talking about dementia because dementia really scares people. Most people have had contact with somebody with advanced dementia and worry about getting that themselves. And I think it’s a really good opportunity to stress these basic things that people can do to really minimize their risk.
Narrator:
Welcome to Medication Talk, an official podcast of TRC Healthcare, home of Pharmacist’s Letter, Prescriber Insights, and the most trusted clinical resources. Proud to be celebrating 40 years of unbiased evidence and recommendations. On today’s episode, listen in as our expert panel discusses medications for the treatment of Alzheimer’s dementia. They’ll review the risks and benefits of cholinesterase inhibitors, memantine, and the anti-amyloid and monoclonal antibodies. And you’ll hear strategies for managing behavioral and psychological symptoms of dementia. We have several exciting special guests on this episode, including Dr. Tatyana Gurvich, Associate Professor at the USC Mann School of Pharmacy, Dr. Candice Pierce, Course Development Manager and Nurse Planner at Elite Learning, and Dr. Darlene Moyer, Associate Director of Honor Health Family Medicine Residency Program and Clinical Associate Professor of Family Medicine and Geriatric Medicine at the University of Arizona College of Medicine. You’ll also hear practical advice from panelists on TRC’s Editorial Advisory Board, Dr. Stephen Carrick from the USC School of Medicine, Greenville, and Dr. Craig Williams from the Oregon Health and Science University. This podcast is an excerpt from one of TRC’s monthly live CE webinars. Each month, experts and frontline providers discuss and debate challenges in practice, evidence-based practice recommendations, and other topics relevant to our subscribers.
CE Narrator:
And now, the CE information.
Narrator:
This podcast offers continuing education credit for pharmacists, pharmacy technicians, physicians, and nurses. Please 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. None of the speakers have anything to disclose. Now let’s join TRC editor Dr. Sara Klockars and start our discussion.
Sara Klockars:
So Craig, we’d like for you to jump in and share with us what some of the brain changes are that occur in Alzheimer’s disease so we can talk about the medications and where they might work down the road.
Craig Williams:
Yeah, no, it’s a good question. Obviously, in applied pharmacology, the goal is always to understand the physiology and then develop therapies that directly treat the physiology. And it’s been challenging in Alzheimer’s dementia. So the two major kind of changes that we know about in the brain structure and has been identified now for a couple of decades are the increasing in amyloid beta plaques and then increasing in these tau protein tangles. And There’s just a nice paper about a year ago out of a group in China that’s doing a longitudinal following of older adults in that country and actually doing some intermittent sampling of cerebral spinal fluid and kind of looking for when changes occur and how they progress. And so they’ve kind of nicely shown that these start well over two decades before any kind of detectable cognitive changes with maybe amyloid beta changes preceding tau. It’s kind of unknown. But unfortunately, while the correlation is strong, the The causation is still hard to prove, but those are two structural changes. The other aspect mentioned there is known changes in neurotransmitter concentrations, the way neurotransmitters behave in these patients’ brains, and whether or not any of those are directly related to the kind of physical changes mentioned is also not real clear. But there’s definitely decreased signaling via acetylcholine, and that plays a fundamental role in all kinds of signaling in the brain. And then a relative excess of excitatory signals transmission, so mostly through glutamate, as noted there. So it’s still a not real understood imbalance. But as we’ll get a chance to discuss, medications have been marginally successful in addressing those changes. The neurotransmitter changes have been less successful in trying to address the physical changes to slow the progression of the disease.
Sara Klockars:
Thank you for that. And you had mentioned some of those changes you know, happen decades before we start to see any symptoms. So Tatyana, could you review the progression of Alzheimer’s disease for us?
Tatyana Gurvich:
Sure. So it is truly a progression. You start with preclinical phase, which is basically no symptoms that anybody can notice. And that transitions to mild cognitive impairment. This stage can last up to five years, and sometimes it progresses to dementia, and sometimes it doesn’t. Generally speaking, patients have mild symptoms. They may have very mild changes in memory, or symptoms will be amnestic in nature. Sometimes there’s slight changes in executive dysfunction, so more issues with planning things. And with more substantial testing, neuropsych testing, you can actually pick up mild cognitive impairment a lot more frequently than with sort of traditional kind of screening tools that we have. So after mild cognitive impairment, sometimes the disease progresses into various stages of dementia. So that will be mild dementia, moderate dementia, and severe dementia. And with mild dementia, you begin to see problems with some daily activities and they kind of progress as you go from mild, moderate to severe. In the mild cognitive impairment stage, there is evidence of pathology. So you do notice the biomarkers like the beta amyloid plaques and the tau protein and that’s why some of these monoclonal antibodies that just came out are effective, were more effective in the earlier stages like mild cognitive impairment and mild dementia.
Sara Klockars:
Thanks for that background. Craig, could you give us a high-level overview of the meds that impact cognition and memory and how they work? And then we’ll get to behaviors in a bit.
Craig Williams:
We have had some modest success in addressing the current neurotransmitter changes. So the cholinesterase inhibitors is probably most commonly known to most listeners and readers of donepezil. These can inhibit the enzyme that breaks down acetylcholine. Acetylcholine, again, plays that complex role in central neurotransmission, but does seem to help focus and help cognition a bit. So restoring some cholinergic function to the cerebral cortex and the brain. And those, again, we’ll talk a bit more about how effective they are and kind of where we use them in therapy, but directly increasing acetylcholine function. As disease progresses, and memantine ‘s
Craig Williams:
been around now for just over two decades, but it’s an NMDA blocker. NMDA is one of the receptors for glutamate, that stimulatory neurotransmitter. So idea there being it’s a modest blocker. So we have more potent blockers of NMDA that have untoward effects. But in this case, we’re using kind of a modest blocker to presumably take the foot off the accelerator a bit to the overactive neurotransmitter. So again, not real well worked out how the physiology in the brain kind of corresponds to improvements in symptoms. But so we can increase the lack of acetylcholine and we can somewhat damp down the excess glutamate with the two major classes we have with the Thank you. Thank you.
Sara Klockars:
Darlene, would you want to comment just on how the anti-amyloid monoclonal antibodies are thought to work?
Darlene Moyer:
So, you know, the idea is that your immune system is trying to go in and clear out the amyloid plaques. And that, as Craig was saying, really leads to the risks of the medication as well, because I know we’ll talk about this down the line some, but the biggest risk is that anytime you’re creating this inflammatory response and attacking something in sensitive tissue, you can then start to have some damage and some bleeding and some edema, which is what leads to the side effects that we’re seeing on the MRI change. and having some bleeding in the brain, which is obviously never a good thing.
Sara Klockars:
Thank you for that high-level overview of the meds we have available for treating cognitive symptoms of Alzheimer dementia. So let’s move along and talk about the role of the meds, dig into some specifics, and then answer some questions from our listeners. And so, Tatyana, I was hoping you could review with us some of the common meds that we should be avoiding in patients with dementia.
Tatyana Gurvich:
Those are all of your anticholinergic meds. So anything with any kind of anticholinergic profile, your old tricyclic antidepressants, for example, some of the atypical antipsychotics like olanzapine, a bunch of OTC drugs like diphenhydramine, doxylamine, other antihistamines like hydroxyzine that we often use for itching and some psychiatrists use it for anxiety, things like urine antispasmodics, the worst one being oxybutynin, but also some of the newer ones also like Vesicare and Enablex, Detrol, even those have significant anticholinergic profile. GI antispasmodics that we would use in our patients with like IBS, for example, with a predominant symptom of diarrhea, all of those medications have anticholinergic profile. Something like Lomotil that we would use for diarrhea has atropine in it, which is anticholinergic muscle relaxants like cyclobenzaprine actually are relative of a tricyclic antidepressant structurally. Paroxetine, which is a SSRI, and we don’t think of SSRIs as having anticholinergic burden, but paroxetine does. Some of the other things that can contribute to confusion and cognitive impairment are things like benzodiazepines. Certainly can cause confusion and cognitive slippage. Things like the Z drugs, Ambien, Lunesta, Sonata are also on the list. And then you have to look at things like cocktails, CNS active cocktails. When they’re taking a bunch of different drugs that affect the CNS, are they going to have slower speed of processing? Is that going to impair cognitive function in those patients? And then you have to look at alcohol and cannabis. I mean, in my patient population, there are all kinds of older adults who want to use cannabis for all kinds of reasons. But at this point, I don’t know that there’s that much research in the frail older patients and the use of cannabis. We’ve seen a number of cases of patients coming in with significant cannabis use and cognitive impairment as well. And of course, alcohol. The amount of alcohol an older adult can drink safely is significantly less than it was when they were younger, for example. So all those things have to be looked at as reversible causes. And these are super easy to get rid of. And hopefully, your mind clears up a little bit
Sara Klockars:
Excellent. And we can help find safer alternatives. Would you want to comment on consideration? So how do you decide which medication to choose?
Tatyana Gurvich:
Sure. So typically for mild dementia, mild to moderate dementia, you would first start probably a cholinesterase inhibitor. Which of the cholinesterase inhibitors you start, I don’t know that it makes a whole lot of difference. In my practice, we use a lot of donepezil. It’s relatively easy to administer. 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, and you monitor for side effects. So the biggest issue with the cholinesterase inhibitor are its side effects. So you can get these cholinergic kinds of symptoms like diarrhea, urinary frequency. And if you’re dealing with an older, frail adult, that could easily translate into urinary incontinence. And that’s a huge life-stopping kind of an event, right? You want to make sure they’re not having a significant bradycardia. So a pulse in the 50s is probably okay, but less than that is probably problematic. You’re also looking for an exacerbation of agitation or worsening of symptoms when you first start the medication. So you’re looking at all of that. And if the patient tolerates it, okay, you can go from 5 to 10 milligrams pretty easily. Donepezil also comes in a higher strength dose of 23 in our experience. In my clinic, at least, we never use it. I think the higher dose just translates into more cholinergic side effects, which patients can’t always tolerate. The other thing you’re looking for with a cholinesterase inhibitor is because it’s cholinergic, you’re going to get watery eyes, runny nose, those kinds of symptoms, drooling sometimes. And so patients have runny nose, watery eyes. They think they have allergies. So they run to the pharmacy and buy a diphenhydramine or a chlorpheniramine or a brompheniramine, some kind of an old-style antihistamine, which can actually cause the opposite problem. It can cause cognitive slippage. So you want to make sure they’re not doing that. For more advanced dementia, so moderate to severe dementia, you might introduce memantine, which is an MDA receptor blocker. You can use it in combination with cholinesterase inhibitors or by itself in more severe disease. I think they’re better tolerated. than cholinesterase inhibitors in general, the biggest issue you’re looking for is an increase in agitation when you start the medication. But if that doesn’t happen, overall, they’re tolerated pretty well. Some people will get a little diarrhea. Some people will get insomnia. Some people will get a little dizziness, headaches. But most of the time, they’re tolerated fine. So some of your more advanced dementia patients will be on both cholinesterase inhibitors and memantine. In terms of Dosing formulations like donepezil comes in a patch. Is there a benefit to that? Probably from a compliance standpoint, maybe. But in terms of coverage, insurance coverage? I don’t know of a Medicare Part D plan that will cover a patch. Rivastigmine is another cholinesterase inhibitor that we sometimes use. It comes as pills and patches. I think the reason they developed a patch is because in oral form, they were so poorly tolerated and had so many cholinergic kinds of side effects that the only way you can tolerate rivastigmine is with a patch. So sometimes we use that if patients have trouble swallowing or don’t like to take pills. But those are the two that we mostly use donepezil, 5 to 10 milligrams, or rivastigmine, usually in patch form, and then a combination of them for more advanced disease and usually cholinesterase inhibitors for milder symptoms.
Sara Klockars:
Thank you for that. Darlene, what do you most commonly use in practice?
Darlene Moyer:
I think that was a great summary. I most commonly use donepezil as well, just because it’s most available, it’s fairly inexpensive, and it’s the one, you know, frankly, that we’re most familiar with. And I think I start to move to patch form of rivastigmine if somebody’s having, you know, a lot of GI upset with donepezil, or if just from a compliance standpoint or, you know, ability to swallow medications, they need to be up on a patch for those reasons.
Sara Klockars:
And I know there was recently a new prescription approved, Benz- galantamine. Do you see that as having a role? I
Tatyana Gurvich:
saw galantamine used when it first came out when I was actually in a family practice residency program. Some neurologists were prescribing it, and we would get patients on them. But since I’ve been in my geriatrics practice, we don’t have a single patient on galantamine, and certainly not on that new one. With Medicare Part D coverage, issues, especially this year, I cannot imagine that it’s going to be covered at all, and certainly not anytime soon. I don’t know what everybody else thinks.
Darlene Moyer:
I’ll be honest, I haven’t used this at all. And, you know, when I looked it up to review it, I understand it’s only twice a day dosing as well, which just from a ease of administration standpoint is really difficult for patients.
Sara Klockars:
Thank you. And so when starting these medications, we kind of talked about some of the considerations and side effects and risks. Can you share a conversation that you have had with a patient or a caregiver regarding the benefits of these medications and the realistic expectations that they can see in their day-to-day life?
Tatyana Gurvich:
So The conversation I have with my patients is that whether you’re starting donepezil or memantine, what these drugs generally do is delay the progression of symptoms and delay the progression of the dementia. So a lot of the times when you start these medications, you really, if you notice no change, that for a long period of time, that probably means the drug is working. I think if they’re expecting to see an improvement in cognition or daily activities, I think that may be an unrealistic expectation. So most of the time, you kind of see no change and you’re stable at the level you were prior to starting the medication. I do go over all the side effects and making sure that they know how to deal with them and if they develop side effects that they just can’t manage and like incontinence being one of them to come back and we can talk about options. Sometimes they’re on a higher dose of donepezil, you back off a little bit to the lower dose to see if that improves things. Sometimes you add memantine a little bit earlier, that happens. Family members, patients, caregivers have to realize the limitations of these drugs, that they’re not going to necessarily make the patient better, they may probably just keep them at the level they’re at, longer.
Sara Klockars:
Does anyone else want to chime in about common misconceptions some of your patients have had about these medications?
Darlene Moyer:
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 that part, it makes it easier to have the conversation about medication expectations, because sometimes pausing those symptoms, like Tatiana was saying, or even if you can at very best turn the clock back by about six months or so, that might be a great thing. And that might actually buy patients and families time when they’re trying to make decisions about needing to look into other living situations, looking into assisted living or memory care centers. Even a little bit of extra time might be helpful, but But I always make sure that they clearly understand that this is still going to be a progressive disease, whether or not we use the medications.
Candace Pierce:
I absolutely agree that education is so important. When we first start having these conversations with families, This is a time that it is very hard for them to really latch on and understand what you’re saying because they’re just trying to digest the fact that they’ve received this diagnosis and their whole world is about to change and all their roles are about to shift. And so I find that having these conversations, just little reminders as they’re coming in for appointments and is really good so that it’s not so overwhelming for the family.
Sara Klockars:
Thank you. And another question we have had from subscribers is, so if patients are starting on these anti-amyloid monoclonal antibodies for early onset or mild cognitive impairment, can we add cholinesterase inhibitors or memantine to those antibodies?
Darlene Moyer:
Yes, you can. Most of the patients right now that are getting these monoclonal antibodies are part of a trial or are at a big research center. So if you’re going to be the one outside of that center making changes to their medications, you would always want to communicate with the team that was overseeing the protocol that they were enrolled with. But yes, you can use them. And actually, most of the studies are being done in patients who are already on medications for dementia as well.
Sara Klockars:
Thank you. And then another question that’s come up is, when do you consider stopping medications for dementia? And are there risks with stopping these medications? So how do you approach deprescribing with the patient and caregiver?
Tatyana Gurvich:
So some of the reasons to discontinue would be if they’re non-adherent, if they’re not taking it on a regular basis, if there’s continued deterioration despite being on medications, if there’s sudden increase in comorbidities and it just makes it more difficult to manage another medication, or if there’s drug interactions that occur with the current regimen. And also, you want to get patient input, if possible, caregiver input, family input. Sometimes it’s their decision to decide to stop. I think if the patient is stable and is not experiencing a decline, I think it’s worth it to continue because sometimes what we do see is when you stop a medication and they do kind of regress a little bit more quickly, and then when you restart the med, it’s hard to bring it back up to that level. I think that would be the only risk of stopping the medicine, that a patient could significantly decline shortly after the But if there is a decline in function and cognition anyway, and it becomes more cumbersome to take the medicine, then I think it is okay to discontinue it.
Sara Klockars:
And can patients just stop them, or do they need to taper them?
Tatyana Gurvich:
They should be tapered over some time. Usually, like if you’re on an episode 10, you should probably go to 5 for about a month and then see how you do, and then you discontinue. So they shouldn’t be abruptly discontinued.
Craig Williams:
Yeah, if you’re on anything but the starting dose, then moving down is a good idea. So although to the earlier comment, often five of donepezil is a dose patients are on when we’re seeing them. So in which case there’s no further tapering down to do.
Sara Klockars:
Thank you. What are some of those dementia behaviors that we may see and non-drug measures to consider for managing those?
Candace Pierce:
Your non-drug measures are really going to focus on promoting physical and emotional comfort. You have a lot of symptoms that come with dementia from agitation and aggression, and a lot of times We want to try to make adjustments to our environment to reduce that aggression and agitation and confusion that they’re going through. And so that can be things as simple as minimizing noise, getting rid of the clutter, even adequate lighting. If the lighting is too bright and just overstimulating, it really overwhelms their senses. So you really want to work on creating a calm environment and also structured routines for activities like their eating, their toileting, their sleeping, because that’s going to create that stability and also help reduce some of that anxiety, which is going to, of course, reduce agitation and aggression. Some of the other things that they do as well as you can do, we use the word therapy a lot. So music therapy, white therapy, aromatherapy, things that are calming and soothing to them. There’s also cognitive stimulation that’s really important as well. So having those structured interactions and those daily routines, the goal there is really just to try to preserve the patient’s abilities and even to help them draw out some of their memories as long as possible and making those connections in their brains. And a lot of the caregivers can be trained and receive education on how to interact with their loved one through these different types of, you know, there’s validation therapy, reminiscent therapy to really help with that. So I do encourage a lot of the caregivers to try to work on creating these routines and, you know, what are some of the things that their loved one enjoy doing and how can we put that into their day?
Sara Klockars:
Stephen, did you have anything else to add, or do you want to comment on some other meds you may see or use for dementia-related behavioral or psychological symptoms?
Stephen Carek:
Yeah, I mean, primary, at least assistance is with a lot of these non-drug therapies, but we’ll use some other medications to hopefully help address some of those disruptive behaviors or tendencies that we’re seeing from our patients. I think one thing is trying to address underlying pain. I think it’s one thing we tend to think about when we’re dealing with patients who may be confused or behaviors may be significantly deviating from what their previous patterns may be. And we know that chronic pain may exacerbate some of these dementia-oriented papers as well. I think it’s one of the things that the top of the list is Tylenol and whether Tylenol can help with some of these dementia behaviors in helping address maybe to calm down some of those pain symptoms that patients may have. There’s also other medications like antidepressants for some mood-related symptoms. We also, I mean, all these medicines as we continue forward. antipsychotics, mood-stabilizing medicines, approaching those patients and trying to address what is the hope with these medications and helping either address or augment the dementia medications that we’re utilizing, but also weighing the side effects from them. Because many of these list medications are also on the BEERS list. Utilizing some of these, especially like antipsychotics, may increase risk for mortality. Really, really strongly considering those risk and benefits is really important when trying to address some of those other behaviors that are not being controlled or managed well with some of their dementia medicines they may be currently on.
Craig Williams:
Yeah, I’ll just add, Sarah, briefly, we discuss all the time that generally we have lots of medications that make dementia and cognition worse and not a lot that make them better. So we’ve talked a lot about taking a holistic approach to these medications, to patients’ medication lists, looking for things that may be exacerbating adverse effects of therapies we want to keep on board you can get rid of and But also just recognizing that a lot of things get added by providers that may not be taking care of the cognitive aspects of the patient can worsen things. So just being very alert to that med list. And yeah, so many things can, the whole list of medications talked about, you try to avoid early disease to just kind of make it worse later on.
Tatyana Gurvich:
Can I just add to that? So when you’re talking about trying antipsychotics, like People said there is this black box warning for increased risk of mortality. with them. And so when you’re talking about agitation, I think it’s really important to identify specific behaviors that patients are experiencing. Because, you know, agitation to me could mean one thing, to a caregiver it could mean something else, or really agitation exhibited by. And the behavior has to be a danger to the patient or a danger to the caregiver. If that’s the case, then antipsychotics at low doses may be appropriate. But you have to kind of hone in on that behavior. And as you’re titrating up the dose gradually to see if the behavior goes away. These drugs aren’t effective in all patients. And in fact, a lot of times they’re ineffective. And so you have to decide when to treat and how to treat and kind of monitor the treatment carefully to make sure it’s effective and doesn’t produce adverse events.
Craig Williams:
Yeah, it’s a great reminder. They’re for the agitation. They’re not for the cognition. So they They do not improve cognition, it’s just for agitation. So yeah, it’s a great point that what is agitating them and can we do anything else to mitigate the need or less the need for an antipsychotic knowing it’s not going to help the end-of-line disease process.
Sara Klockars:
So let’s just transition really quick to dementia risk reduction. What are some strategies you recommend or that have evidence to support reducing the risk of cognitive decline?
Stephen Carek:
I think some of the big risk factors that we address, especially if we can address early in life, early adulthood through middle age, healthy weight, really focusing on things like regular physical activity, exercise, managing those comorbidities of high blood pressure, diabetes, limiting substances that may affect cognition, especially with chronic and damaging use like alcohol, tobacco cessation. Other things that I really like talking about too is sleep with patients. I think sleep is a huge, I think poor sleep and dysfunctional sleep is also a significant risk factor for developing dementia later in life. So really trying to identify patients who have sleep apnea, intervene, but really helping patients develop good sleep hygiene habits. I know there’s some theory behind the glymphatic system and being able to help reduce sort of the tau buildup that may occur and cause dementia and sleep, and the glymphatic system can be a huge process in that. But encouraging just overall holistically healthy lifestyles, promoting healthy behaviors like healthy diet, healthy exercise and physical activity patterns, and reducing those toxic or damaging substances, namely alcohol, tobacco,
Darlene Moyer:
I agree. I really love this topic because I think it’s an opportunity to really grab people’s attention about the importance of these healthy lifestyle factors. And then the benefit is that these things also are all items that help promote healthy aging, maintenance of physical function over time, and all the other parts of aging that we want to improve for people as well.
Sara Klockars:
Thank you. I have one last subscriber question. So do GLP-1 agonists have a role in dementia?
Darlene Moyer:
I have not yet heard any definitive evidence one way or the other. I suspect over the next couple of years we’ll have lots of studies and hopefully get some good answers for this. But so far, I haven’t heard any compelling evidence one way or the other.
Stephen Carek:
The best theory I’ve had would be GLP-1s do so much. And I think there’s a central theory of the inflammatory reduction that occurs with GLP-1s may be driven by a lot of the weight loss and especially leading to obesity being maybe also a disease of chronic inflammation. Through that, is there a possibility? Maybe, yes. But again, the evidence is not there yet. But there could be some promising data that could help support that.
Narrator:
We hope you enjoyed and gained practical insights from listening into this discussion. Now that you’ve listened, pharmacists, pharmacy technicians, physicians, and nurses can receive CE credit. Just log into 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. On those websites, you’ll also be able to access and print out additional materials on this topic, like charts and other quick reference tools. If you’re not yet a pharmacist’s letter, pharmacy technician’s letter, or Prescriber Insight subscriber, find out more about our product offerings at trchealthcare.com. Be sure to follow our subscribe, rate, and review this show in your favorite podcast app, or find the show on YouTube by searching for TRC Healthcare or clicking the link in the show notes. You can also reach out to provide feedback or make suggestions by emailing us at [email protected]. Thanks for listening to Medication Talk.
Medication Talk
