Breaking Through Biases in Obesity Management: Building Competence, Creating Connections, and Empowering Leaders in Primary Care

Chair, Angela Fitch, MD, FACP, FOMA, Jaime Almandoz, MD, MBA, FTOS, and Carolynn Francavilla, MD, DABOM, FOMA, discuss obesity in this CME/NCPD/AAPA activity titled “Breaking Through Biases in Obesity Management: Building Competence, Creating Connections, and Empowering Leaders in Primary Care.” For the full presentation, downloadable Practice Aids, and complete CME/NCPD/AAPA information, and to apply for credit, please visit us at https://bit.ly/3YYA4bF. CME/NCPD/AAPA credit will be available until March 10, 2026.

1. Dialing Up the Power
of Alzheimer’s Disease Biomarkers

A Practical Pathway to Earlier Diagnosis

El

Alireza Atri MD, PhD Scott Kaiser, MD

Chief Medical Officer, Banner Research CEO, Determined Health

Banner Alzheimer's & Research Institutes k Director, Geriatrie Cognitive Health,
(Phoenix, Tucson, & Sun City, AZ) Pacific Brain Health Center
Director, Banner Sun Health Research Institute ‘Adjunct Professor, USC Leonard Davis
(Sun City, AZ) School of Gerontology

Banner Health Los Angeles, California

Phoenix, Arizona

Lecturer on Neurology

Center for Brain/Mind Medicine,

Department of Neurology

Brigham and Women's Hospital

Harvard Medical School

Boston, Massachusetts

Go online to access full CME/MOC/AAPA information, including faculty disclosures.

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2. Our Goals for Today

Equip you with skills to evaluate the relevance of different
fluid and imaging biomarkers to assess AD pathology

Offer strategies to integrate biomarker testing into your
clinical practice to inform AD diagnosis and management

Provide guidance on the principles of shared decision-
making to facilitate patient and care partner understanding of
the role of biomarker testing in an AD diagnosis

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3. Module 1
Biomarker Basics
Essential Concepts for AD Diagnosis

and Management

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4. Why Is It Important for Patients to Receive
a Timely and Accurate Diagnosis of AD?17

Atimely diagnosis
An accurate allows patients the

diagnosis validates an
patient and family shared decision-
concerns with a making about their
specific diagnosis care while they are
still capable

Recently approved
and emerging
disease-modifying
therapies are only
indicated for
patients with early-
stage AD, and
biomarker
confirmation is
required for
treatment

1. Cummings Jet al. J Prey Alzheimers Dis. 2023, 10:362-377. 2. van Dyck et al N Engl J Med. 2023 388:9-21. 9. Legembi (lecanemab) Prescribing Information

ps nw accessdata fa goverupsatida_docs/labe/2023/761268013 150011 pt. 4 Kisunla (donanemab) Presenbing Information
ps av accessdeta (da gowcrugsatda_docssabeV202476124850000 paf. 5. Sims Jet al. JAMA, 2023,330:512-927.

6. Liss Letal. J Intern Med 2021:200'310394. 7. Porstinsson AP etal. J Prev Alzheimers Di. 2021:3:371-386.

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Copyright ©

5. D Pa

logical Processes T

+ AD is a biological
disease that begins
decades before the

onset of cognitive He ‘iid conte
impairment symptoms in molecular impairment

+ The time BEFORE MCI YY

is the prevention period
Birth 20+ years (?) 6+ years (?) 1-2 years 10 years Death

Time, y

First potential detection of
pathological brain changes

+. Dolioyan NY ela Alzheimers Dement 20228012390. PeerView

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6. Updated Biomarker Categorization From the Revised Criteria

for Diagnosis and Staging of AD (2024)!

Biomarker Categ

CSF or Plasma Analytes Imaging
Core 1 Biomarkers

A (AB proteinopathy) _ ANA PET
‘AB42/AB40, p-tau217,

T, (phosphorylated and

secreted AD tau) p-tau181/AB42, -

p-tau217/np-tau217, t-tau/A642
Core 2 Biomarkers

P-tau205, MTBR-tau243,
np-tau fragments

Biomarkers of Nonspecific Processes Involved in AD Pathophysiology
N (injury, dysfunction, or degeneration

T2 (AD tau proteinopathy) Tau PET

of neuropil) NfL Anatomic MRI, FOG PET
1 (inflammation) astrocytic activation GFAP -
Biomarkers of Non-AD Copathology
V (vascular brain injury) - Infarction on MRI or CT, WMH
S (a-synuclein) aSyn-SAA -
duc GR al Azheimers Dont. 202420514510 PeerView

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7. urrent Indications for Clinical AD Biomarker Testing

Clinical AD biomarker testing is indicated for patients who are undergoing an
evaluation who have objective evidence of cognitive impairment (biomarker
testing is not recommended for individuals who are not cognitively impaired at this
time), and

1. Inwhom AD is a potential cause of cognitive impairment,
2. AND biomarker testing is expected to affect diagnosis and/or management by
a. Improving the accuracy of a dementia diagnosist-3

b. And/or determining whether patients may be candidates for AD-specific
treatments, such as anti-amyloid antibodies*

1. son KA et al. Mzheimers Dement 201.106 e108, 2. Shaw LM eal Alzheimers Dement 2018:16:15051821, 9. Hanson O etal Alzheimers Dement. = Dear jew
2022.18:2869-2688, 4. Cummings Jet al. J Prev Alzheimers Dis. 2023,10.362-377.

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8. Clinically Available Alzheimer’s Disease Biomarker Tests
14

MN Amyloid PET AIM CSF tests m= Blood tests

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9. Amyloid PET'$

+ Procedure ‘Amyloid PET Negative
~ Patient is injected with a radiotracer that binds amyloid plaques
— PET scan images the radiotracer binding

+ Interpretation: visually read as “positive” or “negative”; some centers can
also provide continuous values (Centiloids)

+ Visualizes the burden and distribution of amyloid plaques
Advantages + FDA-approved and now covered by Medicare

+ Considered a “gold standard” for amyloid pathology and can track ‘Amyloid PET Positive
amyloid plaque removal by anti-amyloid treatments

+ Requires expensive, specialized equipment and highly \
trained personnel

+ Cost is typically >$6,000/scan, and commercial insurance
may not cover it

+ Requires radioactivity

1. Wong DF etal. J Nucl Med. 2010:51913:920.2. Rabinouci GO et al JAMA, 2019:321:1286-1284, 3. Je CVM etal Pharmaceuteals.2021:14:110.
4. Chövez-Fumagall MA et a J Alzheimer’s Dis Rep, 2021:5 1530.5. hitos/hvw cms gowMedicare-coverage-dalabase/viewincaceldecison- PeerView
‘memo aspr7proposed=NENCALd=308. 6. Schindler SE et al. Nat Rev Neurol 202420426438.

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10. + Procedure
- Patient undergoes a LP to collect CSF

— Concentrations of certain proteins in the CSF (eg, AB42, AB40,
p-tau181, total tau) are measured

Brom

Doom

SE ie " Brom —
+ Interpretation: positive, negative, or intermediate based on the a
cutoff value for a ratio; continuous values provided een

+ Tests for non-AD conditions can be performed
+ FDA-approved
+ Covered by insurance
+ Concurrent APOE genotype testing can
be performed

+ Most patients have never undergone LP, and
some refuse due to perceived risks

+ Some contraindications to LP

+ Time-consuming and expensive to train staff, set
up LP clinics, and perform

4. Duts FHet al. Alzheimers Dement. 2016:12:154-163. 2 BltnerT eta. Alzheimers Dement 2016:12:517-526, 3, Janeliize Set al, Ann Cin Trans! Newt PeerView
2016.3.154-185. 4. Canevell Metal Front Aging Neurosci. 2019:11.282. 5. Schindler SE el al Nal Rev Neu. 2024.20:428439.

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11. Blood Biomarkers!7

+ Procedure
— Patient undergoes a blood draw
- Concentrations of certain proteins in the plasma/serum (eg, Aß42, AB40, p-tau217) are measured
+ Interpretation: positive, negative, or intermediate based on the cutoff value; continuous values provided

+ More acceptable, more accessible, less burdensome, and less
expensive than other modalities

+ Variability in the accuracy of various AD blood tests

+ Lack of reimbursement or inconsistent reimbursement

+ Some tests may not perform consistently in all groups or in patients
with certain comorbidities (eg, kidney disease)

+ Current tests may not reflect amyloid clearance on an individual level

1. QUY etal Neurosci Blobehav Rev. 2021:128:478-406 2 LY et al Neurology. 2022.38:0688-659, 3. Jack CR ei al. Alzheimer's Dement 2024;1-27
4 Been etal Prac New, 2024237782 5 Harpe tal won DEDOS. 6, Deverk PA et al. JAMA, 2028;382:1877-1878, PeerView
7. Schindler SE et al. Nat Rev Neural 2024:20 426-4

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12. Highly Accurate AD Blood Tests Are Clinically Available Now’?

AG PET Positivit
Anz 1000) ee CL"
10 a
bon olaaa
2 CSFpaautt”
i os
ae CSF AR42/40!
o
10 075 05 025 0 050807080910 050807080910
Specificity AUC AUC

ROC Curve for P-tau27 Ro Curve for APS2in Primary Care, ROC Curve for p-tau217

ROC Curve for APS2in Secondary percentage in Primary Care een Percentage in Primary Care

, oe (Prospective Analyses) y (Prospective Analyses) m (Prospective Analyses)
> ¿o =
3 os zos 2
04
ie) à . 5 dal,
02 | Auc 65% ct: 0.87 (035-088) spud asx cy-097 995-098) 02 | auc fos ca: 0.96:0.94-0.98) e AE gon co 0.98 02200)
o o o o
10 08 06 04 02 0 10 ce 06 0% 02 0 10 08 06 de 02 0 19 08 065 04 02 0
Specificity Specificity Specificity ‘Specificity,
+. Barthélemy NR eta. Nat Mod 2024:30:1085-1095.2. Palms Set a JAMA.2024:332:1245-1257. PeerView

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13. AD Blood Tests That Are Clinically Available

Pet
Test Name Assay Type Biomarkers
AB42/40, age, apoE
PrecivityAD, PrecivityAD2' IP-MS proteotype; AB42/40,
p-tau217 %
CertuitAD? Immunoassay P-tau217
à P-tau217, AB42/40,
3
Lumipulse: Immunoassay p-tau217/A842
ALZpathDx* Simoa P-tau217
LucentAD® Simoa P-tau217
IP-MS for AB42/40;
, 0 AB42/40, p-tau181,
E 6 x
AD-Detect‘ immunoassay for p-tau181 p-tau217

and p-tau217

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essineurlogial-dsorders/campeignsiaizheimens-isk.assessment.

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14. Plasma P-tau217 Tests Are Most Accurate’

‘Amyloid PET Early Tau PET Cortical Thickness Cognitive Impairment S FNIH

fi
1% p-tau217 + ABA2AB4O can i -
pai pag 0 E
A BIOMARKERS
2 CONSORTIUM
p27 + ABA2A6A0| jme 1 —
1 +
es
Aa =
sm 1 >
patate ape aguo + GEAP ONL | Roche 1
ptet + A
pin D =
des

PrastB1 + ABAZAA4O + GEAP + NL]
put + ARAZIAGAO

paut61 + ARAZIAGAO + NL]

GFAP

ren

+. Sehinder SE ea Alzheimers Dement, 202,20 6074-8098, PeerView

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15. + Consider minimum acceptable performance
standards for AD blood tests used in clinical care

5 itivi ificit ji | The Alzheimer's Association appropri:
200% sera IN ee ee
[A

em er cur ms

— 290% sensitivity and 275%-85% specificity Bere if
for amyloid PET status for triaging tests

. i ifi Acceptable performance of blood biomarker tests of
Define which specific tests meet these amyloid pathology endete roan the

standards and their appropriate use Global CEO Initiative on Alzheimer’s Disease
(Alzheimer's Association Appropriate Use
Recommendations)

+ Regulatory approval of high-performance
tests, which will likely lead to reimbursement
for these tests

+ Clinician education regarding use of tests

1. Hansson O ell Alzheimers Dement, 2022:18 2660-2686, 2. Schindler SE el Na Rev Nero. 202420.428-439. PeerView

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16. How Are Blood-Based Biomarker Tests Interpreted?"

+ In the example below, the AD biomarker test is assumed to have 90% sensitivity and specificity for

amyloid pathology

+ Test results must be integrated with clinical information for an accurate diagnosis

~ Patients’ pretest probability affects how positive and negative blood tests should be interpreted

Patient Pretest Probability

ent of Amyloid Patholog)

75-year-old patient

98% of patients have a true-positive

61% of patients have a true-negative result

with a typical AD 25 result (have amyloid pathology) (do not have amyloid pathology)
dementia 2% of patients have a false-positive 39% of patients have a false-negative
O result (do not have amyloid pathology) result (have amyloid pathology)

69% of patients have a true-positive 97% of patients have a true-negative result
60-year-old patient result (have amyloid pathology) (do not have amyloid pathology)
with subjective 20

cognitive decline

1. VandeViede L, Schindler SE. Alzheimers Dement 2025 21614201

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31% of patients have a false-positive
result (do not have amyloid pathology)

3% of patients have a false-negative result
(have amyloid pathology)

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17. Module 2
Improving AD Detection
With Biomarker Testing

A Practical Guide for Primary Care
and General Specialty Clinicians

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18. t’s Begin With A Patient Case: Kevin, a 67-Year-Old Man

Initial presentation
and cognitive
assessment

Care partner is
Stacey, his

45-year-old
daughter

Medical and
family history

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is a 67-year-old rei

d software engineer with 18 years of education who presented with
progressive memory decline for the past 18 months

‘Sometimes forgets to do things (eg, set garbage bins out once a week)
Experienced mild confusion with sense of direction in unfamiliar environments and
some word-finding difficulties

Exercises 3x/wk and has a healthy diet

She reported that he has been increasingly repeating himself, forgetting
appointments, and has some difficulty managing finances

She reported independence across ADLs, including shopping, driving, and taking his
own medications

Medical history: hypertension and T2DM, both controlled on medication

(lisinopril, metformin)

Positive family history for dementia: His mother died with dementia at 86 years of
age and his father died of a stroke at 81 years of age

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19. o Should Be Evaluated for Cognitive Impairment?1?

+ Any middle-aged or older patient who self-reports—or whose
spouse, family member/friend, or other clinician reports—concern
regarding symptoms of cognitive, behavioral, or functional decline

+ During the annual wellness visit or any visit in which cognitive
decline may be suspected, ask about cognitive, behavioral, or
functional impairment

— “Do you or others think that you are having trouble
remembering things?”

- “During the past few years, have you or others noticed
changes in your mental abilities?”

— Identify and document care partner information if available

1. Cordell Get al Azheners Dement. 2013::141-150.2. Ati Atal. Alhaners Dement 202100020. 14953. PeerView

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20. Alzheimer’s Association DETeCD-ADRD: Recommendations
for Primary Care and General Specialty Care’

Seven Core Elements of the Evaluation of a Patient With Suspected Cognitive Impairment

1. Establish shared goals for diagnostic process
2. History of present symptoms from patient and care partner

3. Structured multidomain 4. Biopsychosocial history and risk factors
systems review
Cognitive
ADLs
Behaviorneuropsychiatric
Sensorimotor:

+ Developmental history + Risk factors for neurodegenerative and
+ Social history cerebrovascular diseases
OF Heath related behavior Other risk factors for cognitive or

+ Family history behavioral symptoms

6. Integrate information from all cores to develop three-step diagnostic formulation
+ Step 1: Delineate cognitive functional status (CU, SCD, MCI, or dementia mild, moderate,
Mental status exam severe, terminal))
Medical y Step 2: Characterize cognitive-behavioral syndrome (eg, primarily memory [amnestic],
Neurologic language [aphasic))
Psychiatric + Step 3: Determine likely etiology (eg, AD, vascular) and potential contributing factors

(eg, medication or medical conditions)

. Exam

14385, 2. Dikerson BC et a. Alzheimers Dement. 2024 10,1002. 14397.

Copyright © 2000-20:

21. Diagnostic Workup of AD: Testing and Evaluation*3

Brief Cognitive Assessments to Detect Cognitive Impairment or Dementia

Name Mo, MMSE®#*

ET GE E
Time to administer, 25 pabenis
LE 1045 740 740 69 ss
Two suggested: 2880
26:30 has 92% PPV; <2has <S patents
ZN or 212,y of :
dat (1 point added to raw 100% PP for or
Cutoff for potential Cl score 512 y of a = education, 25120 for domentia(62% <& patients and
education) Veh occa sensitiv, <A informants
100% specify)
Sensitivity for Cl, % E El 78 9 8085 85
Specificity for Cl, % 87 2 E 81 8587 ES
Cognitive domains assessed
Complex tention v Y = Y = =
Executive function Y - Y Y y Y
Leaming and memay Y Y Y Y Y Y
Language Y Y = Y Y =
Visual constuction Y Y Y Y e Y
Orientation Y Y - Y Y Y
Available in multiple Ves: Fa Ya o do Yen

index scores can be callate to better inform domain-specific performance. ° Mixed frdings in people wth lo education. <Wel-known among cians. ‘Purchase
required. *Limited evidence fr senstvity to detect mid changes. ‘Simple scoring algorthm. Evidence for sensitiiy to detect mil changes. "Largely studied in veteran

‘populations. 'Prowdes broad range for leaming and memory performance (14 ponis). Limited direct assessment of language-only verbal fueney fer semant animal
Category tested. * Validated in primary care setings.

4 AI A et al. Alzheimers Demen!, 2024 10 1002/az.14335, 2. Ari Aet al. Al2heimers Dement 2024;10.1002/az.14333, 3, Dickerson BC eta. Alzheimers Dement
2024;10. 1000/0. 14937.

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22. Diagnostic Workup of AD: Testing and Evaluation‘ (Cont'd)

Screening Tools to Identify Functional Impairment and Behavioral/Psychiatric Symptoms

Types of Screening Tools Screening Tools That Are Administered to the Patient
ADLs/IADLs
Activities of Daily Living and Instrumental
Functional

Activities of Daily Living
Administer to patient or care partner

A PHQ-9 (depression)
Behaviors NPI-Q (neuropsychiatric and behavioral symptoms)

1. Mos:championstoreath org wp-contentuploads/2021/08/Alzhemers-Project-Bookle-v! 1-08222'-Web pdf. 2. hips un dementiacaeaware orgwp-
contentuploeds/2023/04/UCSF_ADL_IADL_JODAI pdf 3. htps/ww.apa.omidepression-guidelinelpaient-heath-questionnaie pat PeerView
4 his ri cece unc edularcdls seuls pube vs documents MGNPI pd.

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23. Diagnostic Workup of AD: Testing and Evaluation‘ (Cont'd)

+ Lab tests (B12, TSH, homocysteine, CBC with differential, complete metabolic panel
[including calcium, magnesium, liver function tests]), ESR, CRP

+ Brain imaging: MRI (preferred) or CT scan

At this point, clinical and medical history and diagnostic data can be integrated
to make a clinical diagnosis

Is your patient is a candidate for AD biomarker testing?

Y AA tal Alzheimer Dement 2024101002 14353 2 Dieron BC et a. Almeimers Cement 202410 100212 14337. Hann
2. Parstensson AP el al. J Prev Al Ds. 2021;3:371- 388, 4. iA et al. Alzheimer Dement, 202410 1002014935 PeerView

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24. Kevin, a 67-Year-Old Man (Cont’d)

Kevin is a 67-year-old retired software engineer with 18 years of education who presented with
progressive memory decline for the past 18 months

MOCA score: 25/30, which suggests possible MCI (particularly with his
level of education)

Neurological evaluation: normal

Current medications: lisinopril, metformin, aspirin

Lab tests: all normal

MRI findings: mild/moderate bilateral parietal atrophy, moderate medial

frontal atrophy, mild bilateral hippocampal atrophy, mild/moderate small
vessel ischemic disease, 1 lacunar infarct (<1 cm) in the left putamen

joes Kevin need biomarker testi

Diagnostic

workup

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25. Assessing the Need for AD Biomarker
Testing in the New Treatment Era

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26. What Are They and How Do They Work?

+ First disease-modifying therapies to be approved for AD
+ Can lower amyloid plaques substantially; majority of patients become “amyloid negative” within 12 to
18 months of treatment

Impact on Slowing of Clinical Decline

+ Evidence shows slowing of clinical decline by 20% to 40% for the “average” patient when amyloid plaques are
lowered in those in the early stages of AD

+ Treatments provide, “on average,” the equivalent “savings” of about 5 to 7 months of expected decline
compared with placebo over 18 months

Risks Associated With ATTs

+ Infusion reactions and ARIA are the most common AEs

+ ARIA are typically transient, asymptomatic, and resolve on their own, although serious and life-threatening
events rarely can occur

+ Safety monitoring can be costly and burdensome

1. Cumnings Jet al, BoDrugs 2023:36 522.2. Yoon CH et al nor Pham, 2024:15-10 2496/16 S7E7. 3. Sms Jet a. JANA, 2023290512527. ae
4. Cummings Jet al. Altemers Res Ter. 2021,1398.5.van Dyck Cet at N Eng! Med. 2028388 9-21 PeerView

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27. r Patient Needs Al

argeting Therapies
Starting the Process: Practical Steps for Primary Care
and Specialty Care Settings*

siena Step 4

Step 1 Step 2

Referto
dementia
specialist
for
treatment

Order
biomarker
testing if

feasible

Diagnostic workup

to confirm clinical

diagnosis of MCI |} Order lab work and

or mild dementia MRI to rule out
due to AD (ei non-AD ie

D i If patient is
medical history, risk jg and confirm there

interested in
ATTs

factors, physical and are no
neurological exam, |}. contraindications
cognitive, functional, to ATTS
behavioral

Refer to
dementia
specialist,

for
biomarker
testing and
treatment

as ents)

«Specialy care setings inclu general neuclogy, gaie peychiay, and gerri (other nan dementia subapecalysetingo). PeerView

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28. Stage 1: Asymptomatic, biomarker evidence only

Stage 2: Transitional decline: mild detectable change but minimal
impact on daily function

ATtsare | Stage 3: Objective cognitive impairment insufficient to result in
approved for _| significant functional loss (MCI)
patients in
stages 3 and 4 Stage 4: Mild dementia

Stage 5: Moderate dementia

Stage 6: Severe dementia

1. deck CRet al, Azheimers Demet. 2024.27. PeerView

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29. Role of MRI in the Workup
to Evaluate Patient Eligibility for ATTS'#

MRI rules out other non-AD causes of cognitive impairment, including
Cerebrovascular disease
Mass lesions

Traumatic brain injury

The following MRI findings are contraindications for ATTs

Superficial siderosis
Vasogenic edema
Aneurysm

Vascular malformation

+ Cortical infarct

> Extensive diffuse white matter
disease

1. ps;

University Press, 2014. 3. Cummings J etal J Prev Alzheimers Dis. 2023:10:982-977

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sant nlneuetadgyéementiafol cm 2 Dicken 8, AA. Demento:Conprehenaie Pres end Proctezs Oo UK Oxo PRE View

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30. SPIKES Protocol for AD/ADRD Diagnostic Disclosure!

Assess the
Set up patients (and/or patients (and/or GiveKnowledge Address Emotions Strategy and
interview care partners) care partners) and information with empathy summary
Perception Invitation

+ Physicallysetupa + Understandthe = Assess whether + Provderesullsot + Acknowledgethe + Provide a preview
private, uit patents (andior the patent (andior " tesing with emotioalimpact of a management
space care partner's) care partner) would empathy of the diagnosis plan aligned with

+ Verbally setupthe Understanding and like to know the Disclose Provide opportunity the patent and

context and goals appreciation of cause of their syndromic for the patient and care partner's

forthe visit their symptoms symptoms diagnosis, etologic care partnerto goals and needs
Determine if their» Understand what diagnosis, and express their + Discuss folow-up

perception oftheir types of stage emotions pian

symptoms has information they do. Mayalso discuss Offer support + Reassess
eke Gor the in = want to prognosis if understanding
inning of the leam (eg, desired by patient “
evaluaten process dlagnost, sta, feia avan
+ Assess their prognosis) + Invite questions summary of the
knowledge of + Assess the from patient and most relevant
causes of cognitive patients emotional care partner information
decine readiness to
receive the
information
+. Oriental Alheimers Dement. 202421:e14200, PeerView

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31. Are ATTs Right for Your Patient?
Having a Frank Discussion About Treatment-Related Risks’

‘Download the

practice Ale! Patients need to be diagnosed with early, symptomatic AD (eg, MCI or mild dementia due to AD) that is

confirmed with amyloid PET or CSF biomarker testing
ATTs are not + Also need APOE genotype testing
eee or - Patients with one or two copies of APOE £4 are at higher risk of developing ARIA

some patients
+ Baseline MRI findings (eg, microhemonhages, CAA) can indicate elevated risk for ARIA

+ Patients on anticoagulants may not be eligible for ATTS

+ Risks of ARIA and symptoms to watch out for, such as headache, confusion, dizziness, and visual changes
+ What are the possible complications of ARIA?

+ What is the patient s individualized risk profile based on their APOE genotype, baseline MRI brain scan,
‘comorbid medical conditions, and current medications?

Risks of treatment

Commitment! + Significant commitment of time/effort/burden to receive frequent infusions, after the commitment to confirm
burden elevated amyloid via PET or CSF testing, and additional follow-up MRIs to monitor for ARIA

+ How much will treatment cost?
Cost + What are the additional costs associated with treatment (eg, pretreatment evaluations, safety MRIs)?
+ What is the insurance coverage?

1. Day GS ell Neuology. 2022:98519631.2. Ramanan VK el a Newofogy. 2023101942352. PeerView

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32. Tools and Visual Aids for Patient Education’ Downtoad te

Practice aig

1. Mis Nlons-lak-science.0rg/2022/0405/predicing-olzheimers disease the sse-ofnavel-beomarkers. 2. tps ct0a52d991.dvaw.
Sänund.com/9e9633a0baaf7661668a2136c02e2820/200000133-e5668eS6EDIAGREE D-Dementa-Group-Educational-TockBload-Tests p7ph=ci0a32d991.

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P-ct0a52466 1

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33. Biomarker Tes

g for Kevin, a 67-Year-Old Man

Kevin is a 67-year-old retired software engineer with 18 years of education who presented with
progressive memory decline for the past 18 months

+ Diagnosed with MCI suspected due to AD

+ No contraindications for ATTs (MRI looked
fine, he is not on anticoagulants, and he has
no other medical conditions that would exclude
him from treatment)

+ Plasma-based biomarker testing (p-tau217)
was ordered to confirm or exclude AD as the
etiology of his MCI, and the test came back as
abnormal, indicating that he likely has beta
amyloid pathology in his brain associated with
a biological diagnosis of AD

+ Kevin was referred to a dementia specialist for
further evaluation and potential ATT

Biomarker

testing

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Li

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34. Take-Home Messages

+ Availability of DMTs for early-stage AD has increased the sense of urgency around detecting
and diagnosing AD early in the disease course and confirming etiology with biomarker
testing

+ Different biomarker modalities (amyloid PET, CSF, and blood based) each have unique
benefits and challenges to consider

+ Reliability and accuracy of plasma biomarkers are rapidly improving, and some tests may be
ready for more meaningful integration into clinical workflows for the detection of AD
pathology in patients with objective evidence of cognitive impairment

+ Prescreening patients for AD pathology in primary care helps ensure that only appropriate
patients are referred to specialty care for initiation of treatment with ATTs and may help
reduce long wait times to be seen and treated at specialty memory centers

{AA et al. Azheimers Dement 202410 4002/02 14353, 2. Dickerson BC et al, Alzheimer Dement 202410 10022 14397, 3 JokGRetal, Ahemers Cement. Dae rView
2024.1-27. 4. Mieke NM etal. Alzheimers Dement. 2024:20.8216-8224. 5. Vande Viede L. Shindir SE. Alzheimers Dement. 202521614201

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