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Tutorial

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Poll

What potential benefit of new/emerging agents for AAD is most important?

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Increased likelihood of return to non-pharmacological management only
   
Possibility of personalizing treatment
   
Targeted symptom control, possibly reducing neurodegeneration
   
Improved safety profile
   

Tutorial

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Poll

How do you typically monitor the effectiveness of an intervention for AAD?

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Rely on care partner feedback about changes in behaviour
   
Use a standardized agitation scale (e.g. NPI, CMAI)
   
Observe the patient during clinic visits for changes in behaviour
   
A combination of the above
   
 
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Alzheimer's Disease & Dementia, Neurodegenerative Diseases, Psychiatric Disorders CE/CME accredited

touchPANEL DISCUSSION
A visually engaging discussion designed to emulate a ‘live’ panel experience and provide clinicians with practical expert insights to address their clinical challenges. Useful tips below will show how to navigate the activity. Close

Pharmacological management of agitation in Alzheimer’s dementia: Rationale and evidence for new and emerging treatment options

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Learning Objectives

After watching this activity, participants should be better able to:

  • Outline best practice strategies to manage agitation in patients with Alzheimer's dementia, including psychosocial care and pharmacological treatment options
  • Explain the pathophysiology of agitation in Alzheimer's dementia and the rationale for new and emerging pharmacological treatment approaches
  • Evaluate evidence for new and emerging pharmacological therapies for treating agitation in Alzheimer's dementia
Overview

In this activity, three experts consider best practice in the management of agitation in Alzheimer’s dementia and the potential of new pharmacological approaches that target aspects of the underlying pathophysiology. The discussion is guided by pre-canvassed questions provided by healthcare professionals involved in the management of people living with dementia associated with Alzheimer’s disease.

This activity is jointly provided by USF Health and touchIME in collaboration with the Gerontological Society of America (GSA). read more

Target Audience

This activity has been designed to meet the educational needs of Alzheimer’s disease specialists, neurologists, psychiatrists, primary care physicians, specialist nurse practitioners and physician assistants involved in the management of people living with dementia associated with Alzheimer’s disease.

Disclosures

USF Health adheres to the Standards for Integrity and Independence in Accredited Continuing Education. All individuals in a position to influence content have disclosed to USF Health any financial relationship with an ineligible organization. USF Health has reviewed and mitigated all relevant financial relationships related to the content of the activity. The relevant relationships are listed below. All individuals not listed have no relevant financial relationships.

Faculty

Prof. Jeffrey Cummings discloses: Advisory board or panel fees from Acadia, Biogen, Genentech, Grifols, Janssen, Karuna, Otsuka, ReMYND, Roche and Signant Health. Consulting fees from Acadia, Acumen, ALZpath, Artery, Biogen, Biohaven, Bristol Myers Squibb, Eisai, Eli Lilly, EQT Life Sciences (formerly LSP), Fosun, GAP Foundation, Janssen, Karuna, Kinoxis, Lighthouse, Lundbeck, Merck, MoCA Cognition, New Amsterdam Pharma, Novo Nordisk, Optoceutics, Otsuka, Oxford Brain Diagnostics, Praxis, Prothena, ReMYND, Roche, Scottish Brain Sciences, Signant Health, Simcere, Sinaptica, TrueBinding and Vaxxinity. Grants/research support from the National Institute of General Medical Sciences and the National Institute on Aging. Other financial or material support from Neuropsychiatric Inventory (NPI) copyright. Stock/shareholder (self-managed) from Acumen, Alzheon, Artery, Behrens, MedAvante-Prophase and Vaxxinity.

Prof. Krista Lanctôt discloses: Advisory board or panel fees from Bright Minds, Exciva, Lundbeck, Novo Nordisk and Otsuka. Consulting fees from Bristol Myers Squibb, Cerevel Therapeutics, Exciva, Ironshore Pharma, Kondor Pharma (relationship terminated) and Praxis Therapeutics. Grants/research support from Cerevel Therapeutics. Speaker Bureau fees from Eisai Co., Ltd, Lundbeck and Novo Nordisk (all relationships terminated).

Prof. James Galvin discloses: Consulting fees from Biogen, Bristol Myers Squibb, Cognivue, Eisai, Eli Lilly, GE Healthcare, Lundbeck, Roche and Thema Medical.

Touch Medical Contributors

Christina Mackins-Crabtree has no financial interests/relationships or affiliations in relation to this activity.

USF Health Office of Continuing Professional Development and touchIME staff have no financial interests/relationships or affiliations in relation to this activity.

Requirements for Successful Completion

In order to receive credit for this activity, participants must review the content and complete the post-test and evaluation form. Statements of credit are awarded upon successful completion of the post-test and evaluation form.

If you have questions regarding credit please contact cpdsupport@usf.edu 

Accreditations

Physicians

This activity has been planned and implemented in accordance with the accreditation requirements and policies of the Accreditation Council for Continuing Medical Education (ACCME) through a joint providership of USF Health and touchIME. USF Health is accredited by the ACCME to provide continuing medical education for physicians.

USF Health designates this enduring material for a maximum of 0.75 AMA PRA Category 1 CreditTM. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

Advanced Practice Providers

Physician Assistants may claim a maximum of 0.75 Category 1 credits for completing this activity. NCCPA accepts AMA PRA Category 1 CreditTM from organizations accredited by ACCME or a recognized state medical society.

The AANPCP accepts certificates of participation for educational activities approved for AMA PRA Category 1 CreditTM by ACCME-accredited providers. APRNs who participate will receive a certificate of completion commensurate with the extent of their participation.

Date of original release: 30 October 2024. Date credits expire: 30 October 2025.

If you have any questions regarding credit, please contact cpdsupport@usf.edu

 

 

This activity is CE/CME accredited

To obtain the CE/CME credit(s) from this activity, please complete this post-activity test.

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Topics covered in this activity

Alzheimer's Disease & Dementia / Neurodegenerative Diseases / Psychiatric Disorders
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touchPANEL DISCUSSION
Pharmacological management of agitation in Alzheimer’s dementia: Rationale and evidence for new and emerging treatment options
0.75 CE/CME credit

Question 1/5
Following an inadequate response to multiple psychosocial strategies, you initiate a pharmacological approach to address moderate agitation in your patient with Alzheimer’s dementia. How would you monitor the effectiveness of this intervention?

Best practice for monitoring pharmacological interventions includes regularly assessing both the effectiveness (reduction in agitation) and the presence of side effects.1 Standardized tools (such as the Neuropsychiatric Inventory) and input from caregivers or family members help gauge overall progress, and medication adjustments should be based on a careful review of these factors over time.1,2

References

  1. Cummings J, et al. Int Psychogeriatr. 2024;36:251–62.
  2. Sano M, et al. Int Psychogeriatr. 2024;36:238–50.
Question 2/5
Asked about the underlying pathophysiology of agitation in Alzheimer's dementia, how would you best describe it?

Agitation in Alzheimer’s dementia is associated with both neurodegenerative changes and disruptions in neurotransmitter systems.1 Degeneration of the frontal lobe (responsible for behaviour regulation), combined with deficits/dysregulation in neurotransmitters like serotonin and dopamine, leads to behavioural symptoms such as agitation.1,2

References

  1. Liu KL, et al. Ageing Res Rev. 2018;43:99–107.
  2. Senanarong V, et al. Dement Geriatr Cogn Disord. 2004;17:14–20.
Question 3/5
Which of the following statements accurately describes the mechanism or clinical use of new and emerging therapeutics for agitation in Alzheimer's dementia?

AAD, agitation in Alzheimer’s dementia; SSRI, selective serotonin reuptake inhibitor.

Nabilone is a cannabinoid receptor type 1 and 2 partial agonist currently under investigation as a potential treatment for AAD through several potential mechanisms, including neuroprotection.1,2     

Abbreviation

AAD, agitation in Alzheimer’s dementia.  

References

  1. Outen JD, et al. Am J Geriatr Psychiatry. 2021;29:1253–63.
  2. Sherman C, et al. Curr Opin Psychiatry. 2018;31:140–6.
Question 4/5
Your 88-year-old male patient is showing signs of worsening AAD, despite the use of evidence-based non-pharmacologic approaches for the past 6 months. What approved pharmacologic treatment do you suggest?

AAD, agitation in Alzheimer’s dementia.

In May 2023, brexpiprazole was approved by the FDA for the treatment of AAD.1 As of October 2024, it is still the only FDA-approved treatment for AAD. If there is no improvement or worsening of AAD after implementation of evidence-based non-pharmacologic approaches, it is recommended to then consider pharmacologic approaches.2 

 

Abbreviations

AAD, agitation in Alzheimer’s dementia; FDA, US Food and Drug Administration. 

References

  1. FDA news release. Available at: https://bit.ly/3Y8xZJE (accessed 14 October 2024).
  2. Gerontological Society of America. Insights and Implications in Gerontology. August 2023. Available at: https://bit.ly/3HbJQyE (accessed 14 October 2024).
Question 5/5
Which of the following best summarizes the efficacy of dextromethorphan-bupropion (AXS-05) in treating agitation in patients with Alzheimer's disease, based on a recent phase III clinical trial?

CMAI, Cohen-Mansfield Agitation Inventory.

The phase III ACCORD trial showed that AXS-05 significantly reduced agitation symptoms in patients with Alzheimer’s disease compared with placebo. Significant improvements from baseline in CMAI score were seen in the open-label period (p<0.001), as well as substantially delaying the time to relapse of agitation symptoms compared with placebo in responders during the double-blind period.  

Abbreviation

CMAI, Cohen-Mansfield Agitation Inventory. 

Reference

Cummings J, et al. Neurology. 2024;102(17 Suppl. 1):PL5.004

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