TABLE 3.

Characteristics of the models

Characteristic	IPECAD	SveDem	KP	FEM	Herring	ADACE	BASQDEM	MISCAN	Davis	CPEC	Jutkowitz	CEM
Abbreviation	International Pharmacoeconomics Collaboration Alzheimer’s Disease	Swedish Dementia Registry	Kungsholmen Project	Future Elderly Model	(author name)	Alzheimer’s Disease Archimedes condition event simulator	Basque dementia model	MIcrosimulation SCreening ANalysis (Dementia)	(author name)	Care Policy Evaluation Centre	(author name)	n/a
Developer(s) who were present during the workshop	CGa, AG,AK, AW, AS,BW, LJ, RH	AWa, RH	ASa, AW	BTa, JH	WLHa	ATa, JM	JM, MS-G	CBa, IdK	MD, SJ, REa,	RAa, RW, RH	EJ, LMLa, PS	MBa, MH
Reference	21	22	23	30	28	29	32	31	24	25	27	26
Starting in	MCI due to AD	MCI due to AD	MCI due to AD	MCI	MCI due to AD	MCI due to AD	MCI due to AD	MCI due to AD	MCI due to AD	MCI due to AD	Mild dementia	Mild AD dementia
Goal	Decision-analytic	Decision-analytic	Decision-analytic	General population health and policy outcomes	Decision-analytic	Decision-analytic	Decision-analytic	General population health and policy outcomes	Decision-analytic	Decision-analytic	Decision-analytic and general population health and policy outcomes	Decision-analytic
Original aim	Estimate cost-effectiveness of treatment in the predementia AD in a transparent open-source way.	Estimate Costs and QALYs of AD patients across disease progression and illustrate the potential health-economic effects of a hypothetical AD-DMT.	Estimate potential economic impact of DMT in AD.	Estimate health and policy outcomes in the US population. Focused on risk factors, chronic conditions, functional limitations, mortality, and health-related economic outcomes.	Estimate the potential cost-effectivenes of disease-modifying treatments targeting the predementia stages of AD.	Economic evaluation on various interventions through close tracking of disease progression and the related clinical outcomes.	Assess the cost-utility of Souvenaid compared to placebo in patients with prodromal AD under the conditions applied in LipiDiDiet trial.	Evaluate the impact of primary (risk factors), secondary (population screening and treatment), and tertiary (care and cure) prevention strategies on population trends in dementia incidence and mortality.	Estimate annual progression rates across the AD continuum and evaluate the impact of a delay in MCI due to AD on the trajectory of AD dementia and clinical outcomes.	Using the threshold of £20,000 per QALY to estimate the maximum price of a hypothetical therapy which reduces transition to AD, and within AD from stage to stage, by given percentages.	Predict the lifetime US cost of dementia and estimate the cost-effectiveness of nondrug interventions that ameliorate declines in physical function, dementia-related behaviors or rate of nursing home transition.	To assess the cost-effectiveness of a disease modifying treatment in patients with mild to moderate AD.
Model type	cohort state-transition	Cohort state-transition	Cohort state-transition	Dynamic microsimulation	Patient-level simulation	Individual-patient simulation (DICE)	Discrete-event simulation	Population-based microsimulation and time-to-event model	Cohort state-transition	Cohort state-transition	Microsimulation	Cohort state-transition
Characteristics of the data from which the starting population was obtained	See table items ‘progression during MCI’	See table items ‘progression during MCI’	See table items ‘progression during MCI’	Representative U.S. based sample from Health and Retirement Survey	Sampled from characteristics in Vos [2013] (preclinical AD stage 3) and Petersen [2010] MCI	See table items ‘progression during MCI’	LipiDiDiet trial [Soininen, 2017]	(non)amnestic and amyloid positive MCI, onset age calibrated to Rotterdam Study dementia incidence.	See table items ‘progression during MCI’	See table items ‘progression during MCI’	Randomly determined from published US incident statistics and other observational data [Jutkowitz, 2017].	Patients with Mild AD in the community from GERAS study (France, Germany, and UK).
Progression during MCI:
Characteristics of underlying empirical data	U.S. NACC memory clinic setting data from 2005-2017 on 3553 individuals with community-dwelling prevalent and incident MCI due to AD, with cause defined as primary or contributing cause (i.e., 2011 NIA-AA criteria or NINCDS-ADRDA); age range = 60-89).	Estimate [Vos, 2015] based on multi-country (EU/U.S.) memory clinic research setting sample of IWG-1 based diagnosis of prodromal AD-MCI with mean 2.4-year follow-up to AD-type dementia.	Estimate [Vos, 2015] based on multi-country (EU/U.S.) memory clinic research setting sample of IWG-1 based diagnosis of prodromal AD-MCI with mean 2.4-year follow-up to AD-type dementia.	HRS data restricted to starting ages 69-70 (mean 70.1, SD 0.54), of which 39% are male, in both community and nursing homes with MCI (operationalized by TICS score of 7-11 points or proxy judgement).	Symptom levels leading up to dementia: MMSE: U.S. population norms, the French Paquid cohort (9-year study of 215 future AD subjects), and ADNI (398 patients with MCI); NPI: 50 patients with AD and 40 controls; DAD: 196 patients with AD, 70 patients with MCI, and 75 controls.	1735 patient-level data from ADNI dataset collected from 2003 to 2018.	LipiDiDiet trial: memory clinic individuals with prodromal AD, IWG-1 criteria: episodic memory disorder and a positive biomarker (either CSF, MRI, or PET). Mean age = 71, 50% male, of 311 participants. Mean starting MMSE was 26.4, 60% APO-e4.	MCI onset calibrated on dementia incidence = Rotterdam Study dementia [Wolters, 2017] incidence by age (68,367 person-years); MCI duration = pooled 5 memory clinic cohorts (ADC, DESCRIPA, ADNI, AIBL, Gothenburg H70) [Vermunt, 2019], n = 729 (57% female, mean age = 72 (MCI defined as amyloid accumulation and (non)amnestic MCI.	U.S. NACC memory clinic setting data from 2005-2014 on 18,103 individuals in community dwelling and assisted living residences with ≥1 visit while ≥65 years, impaired not MCI, MCI, or dementia and a primary etiologic diagnosis of probable or possible AD. Baseline mean age 76, 57% female, 19% (N = 3370) in MCI due to AD.	Estimate [Vos, 2015] based on multi-country (EU/US) memory clinic research setting sample of IWG-1 based diagnosis of prodromal AD-MCI with mean 2.4-year follow-up to AD-type dementia.	n/a	n/a
Model/function/estimate	Weibull function; mean = 2.7, medium = 2.1, maximum follow-up = 10.4 years.	Observed 3-year survival probability was 50% and converted to 20.6% annual transition probability, applied indefinitely.	Observed 3-year survival probability was 50% and converted to 20.6% annual transition probability, applied indefinitely.	Probit model for 2-year incidence of dementia, conditional on having MCI. We follow natural life-time progression of select individuals in 2-year increments.	Exponential curves: MMSE: baseline value = 1.7 below age- and education-adjusted norms; baseline rate of change = −0.7 per year, annual increase in rate of change = 23.0% (NPI: value = 3.9, rate = 0.9, increase = 24.7% DAD: value = 95.5, rate = −1.46, increase = 38.7%.	Interconnected linear mixed modeling disease equations for key AD biomarkers and various relevant patient-level scales of cognition, behavior, function, and dependence (disease progression is decoupled from AD severity).	Mixed model reproducing CDR-SB progression by rewriting the formula to get a time to event for mild dementia and moderate-severe dementia.	Time-to-event model based on mean MCI duration (male = 4.8, female = 4.0), multiplied by gamma distributed random variable. Onset before 65: Gamma (5, 0.25) Onset 65-69: Gamma (3, 0.4) Onset after 70: Gamma (1.75, 0.7).	multivariate ordered probit for age-specific transition probabilities to each health state, controlling for health state at the prior visit and current age. A covariate for days elapsed since the prior visit was included to adjust for variation in visit frequency.	Observed 3-year survival probability was 50% and converted to 20.6% annual transition probability, applied indefinitely.	n/a	n/a
Input and/or simulation-observed conversion rate from MCI to dementia (year 1–3)	Input: year 1 = 19%, year 2 = 14%, and year 3 and further = 8-9%.	Input: 20.6% (indefinitely).	Input: 20.6% (indefinitely).	Input: 14.6% (2-year horizon).	Observed: from Markov trace model outputs (conditioned on survival): 6.5% in year 1; 17.9% in year 2; 34.5% in year 3.	Observed: from model outputs (18.7% with AD after 2 years).	Observed: 41% at year 2.	Observed: Conversion rate (MCI to dementia) in year 1 = 18%, year 2 = 28%, and year 3 = 13%.	Input (predicted from ordered probit age 66): 76.4% to MCI, 22% to mild AD, 0.1% to moderate AD, < 0.1% to severe AD.	Input: 20.6% (indefinitely).	n/a	n/a
Landing state from MCI to dementia (if model reflects states) or connection of continuous outcomes across disease stages (if model reflects continuous scales).	Landing in 27 states distributed as empirically observed from the Weibull analysis (n = 760; 71% mild) and assumed community-dwelling.	All mild dementia.	All mild dementia.	n/a	Dementia: if MMSE ≤1.5 SD below age- and education-adjusted norms, MMSE annual change ≥0.5 SD faster than age- and education-adjusted norms, and DAD ≤93.	Patients progress to mild AD from MCI due to AD once their estimated CDRSB goes above 4.5 during a model cycle.	Patients experience first mild dementia (CDR-SB cut-off of 4.5), then moderate dementia (CDR-SB cut-off of 9.5).	All in mild dementia.	Mild, moderate, and severe AD landing states as predicted from the ordered probit regression.	All in mild dementia.	n/a	n/a
Progression during dementia:
Characteristics of underlying empirical data	Same data source as for progression in MCI (NACC). 4423 participants (age range = 60-89) with prevalent and incident dementia and AD primary or contributing cause and at least 2 consecutive assessments.	Swedish dementia registry (SveDem) any-type dementia (memory clinic, GP, nursing home); 53,880 persons (2007-2016); baseline age = 80, SD = 7.8; 59% female; MMSE = 20.9) [Handels, 2020; Wimo, 2020].	The transition probabilities including mortality figures from general population-based Kungsholmen project in Sweden [Fratiglioni, 1992; Jonsson, 2011].	n/a (model does not reflect staging of dementia). Progression reflected by mortality (see below).	Published symptom trajectories [Guo, 2014]: MMSE: CERAD and 7 donepezil trials; NPI: donepezil trials; DAD: DADE study (249 community/institution patients with possible/probable AD).	Same data source as for progression in MCI (ADNI).	Same data source as for progression in MCI (LipiDiDiet).	Rotterdam Study dementia incidence and survival by age (68,367 person-years).	Same data source as MCI progression (NACC). All patients in AD health states have diagnosis of dementia at ≥1 visit AND primary etiologic diagnosis of probable or possible AD at any time.	Mild to moderate: assumption on nursing home admission after mean 6 years from diagnosis [Brookmeyer, 2007]; Moderate to severe: NACC 3,852 patients aged 77 possible/probable AD [Spackman, 2012].	U.S. NACC community-dwelling newly diagnosed (incident) individuals with any-type dementia, mean age = 80, 55% male [Jutkowitz, 2017].	1495 patients from GERAS 36-month observational study (FR, DE, UK, 2010) community dwelling, probable AD (NINCDS-ADRDA), MMSE≤26, age 78, 38% mild, 32% moderate, 31% moderately severe/severe [Wimo, 2013].
Model/function/estimate	Three ordered probit functions (3-class MMSE, FAQ, and NPI-Q), each including previous year’s categorized MMSE, FAQ, and NPI-Q. Predicted transitions from each function were multiplied to obtain 27 state transition probability matrix.	Ordered probit on 23,146 annualized transitions, adjusted for etiology (AD-specific), and inverse probability of censoring weights to adjust for selective drop-out.	n/s	n/a	MMSE: piecewise linear regression equation predicting annual change rate; NPI: linear regression predicting change since diagnosis; DAD: linear regression predicting DAD from MMSE and NPI [Guo, 2014].	Same as MCI model/function	Mixed model for CDR-SB progression to mild and moderate-to-severe dementia considering CDR-SB longitudinal data to extrapolate progression to the longer term. Death from dementia and other causes behave as a competitive risk.	Time-to-event model based on mean dementia duration (male: 7.5; female: 9.9) multiplied by a Gamma distributed random variable to introduce random variation between the simulated individuals.	Same as MCI model/function.	Annual transition probability: Mild to moderate = 0.167; moderate to severe = 0.20 (rounded ordered probit predicted probability of 0.214 at average demographics characteristics). No variation by age, time in stage or any other factor.	Mixed regression predicting MMSE, FAQ, and NPI-Q. Monthly nursing home transition probability from Weibull function including MMSE, FAQ, and NPI (exit probability from Medicare data), total nursing home time calibrated to Medicare.	Time to events function for institutionalization and death. Regression function for change over time in MMSE, iADL, and bADL [Belger, 2019; Bond, 2012].
Categorization for mild, moderate, and severe dementia (as applied for the benchmark cross-comparison results tables)	MMSE: mild = 21-30, moderate = 10-20, severe = 0-9; FAQ = 0-8, 9-23, 24-30; NPI-Q = each item≤1, each item≤2, at least one item = 3.	MMSE: mild = 21-30, moderate = 10-20, severe = 0-9.	MMSE: mild = 18-23, moderate =10-17, severe = 0-9.	n/a	n/a	CDRSB: mild = 4.5-9.5, moderate = 9.5-16.5, severe = ≥16.5.	CDR-SB: mild = 4.5-9.5, moderate/severe = > 9.5.	n/a	CDR: mild < 2, moderate = 2, severe = 3.	MMSE: mild = 21-30, moderate = 10-20, severe 0-9.	MMSE: mild = > 19, moderates = 19-10, severe = < 10 (only done for this analysis, model include disease stage in these terms).	MMSE: mild = 21-26, moderate = 15-20, moderately severe/severe = < 15 (only for baseline severity stratification).
Mortality:
Background mortality	Age-specific from 2013 U.S. life table.	Age-specific from 2000-2016 Swedish life table.	n/a	2-year mortality rates from HRS up to 2016, controlling for a broad set of risk factors.	Age- and sex-specific from 2010 U.S. life table.	Age-specific from 2017 U.S. life table.	Time until death from other causes using Gompertz function for each sex and Spanish age mortality rates.	Age-specific life table for 1950 birth cohort.	Not explicitly modeled.	Age-specific from 2016-2018 England life table.	n/a	Time to death based on GERAS data.
MCI-related mortality	Assumed same as background mortality.	Assumed same as background mortality.	Static mortality rate of 73-year-old person from the 2005 Swedish life table.	Included as a predictor in the HRS-based mortality model.	HR applied to background mortality [Wilson, 2009] from Chicago Health and Aging Project.	Assumed same as background mortality.	Assumed same as background mortality.	Assumed same as background mortality.	Health state specific mortality rates estimated using a probit function and the NACC data.	Assumed same n/a as background mortality.	n/a	n/a
Dementia-related mortality	RR reflecting excess mortality in mild, moderate, and severe dementia [Andersen, 2010] Danish population cohort (1990’s) adjusted for age and CDR-staging.	HR based on Weibull survival function by dementia severity (SveDem data); very mild dementia as reference (see dementia progression).	Static severity-specific mortality probability as observed in the KP cohort [Jonsson, 2011]. KP Swedish general population study age 75-78 followed up to 9 years.	Endogenously determined in the microsimulation based on a range of comorbidities and risk factors.	HR applied to background mortality (same source as MCI mortality HR).	RR reflecting excess mortality in mild, moderate, and severe dementia [Andersen, 2010] Danish population cohort (1990’s) adjusted for age and CDR-staging.	Modeled as parameterized time from the onset of moderate-to-severe dementia to death [Dodge, 2003: table SM1].	Mortality due to dementia is determined by the duration of the MCI, and dementia stages).	Health state/severity specific mortality rates estimated using a probit function and the NACC data.	Excess mortality per annum over background mortality in moderate and severe dementia [Brookmeyer, 2007].	Background mortality not separated from dementia-related mortality, total mortality based on age of dementia onset, sex, and race [Mayeda, 2017].	Time to death as function of age, cognition, function, and behavior, based on GERAS data. Model assumed no mortality benefit for the intervention.
Input and/or simulation-observed relative risk for dementia-related mortality	Input: mild (2.92), moderate (3.85), and severe (9.52).	Input: mild (1.3), moderate (2.4), and severe (4.3).	n/s	Input: 2-year risk MCI = 16.5% dementia increases marginal risk by 4.8 percentage points.	Input: MCI due to AD (1.48) and AD dementia (2.84).	Input: mild (2.92), moderate (3.85), and severe (9.52).	Observed: mean survival 9.0 years, representing 29% reduction versus 12.7 years in general population.	Observed: RR dementia per age group: 50-59: 5.0, 60-69: 4.3, 70-79: 4.8, 80-89: 3.2, 90-99: 17	Input (predicted value from probit age 70 relative to MCI): mild (3.29) moderate (6.59) and severe (11.88).	Input: excess to mortality probability is 0.11.	See previous.	See previous.
Treatment effect:
Implementation of effect	MCI to AD-dementia rate was multiplied with 0.70.	MCI to AD-dementia rate was multiplied with 0.70.	MCI to AD-dementia rate was multiplied with 0.70.	MCI to AD-dementia rate was multiplied with 0.70.	30% reduction in annual rates of change for MMSE, NPI, and DAD.	Amyloid level calibrated to obtain 30% reduction in AD conversion rate in 2 years.	Time from MCI to mild or moderate dementia multiplied by 1.3.	MCI duration prolonged with 30% of treatment duration.	Transition rates from MCI to each of AD-dementia states multiplied by 0.70.	MCI to AD dementia rate was multiplied by 0.70.	30% reduction in 5-year proportion of transitioning to moderate dementia.	30% reduction in change in MMSE and ADL over 18 months.
Discontinuation	10% per year up to 5 years or conversion to dementia.	10% per year up to 5 years or conversion to dementia.	n/s	20% every 2 years until dementia conversion, or up to 5 years.	10% per year up to 5 years or conversion to AD dementia.	10% per year up to 5 years or conversion to AD dementia.	Treatment effect disappeared after onset moderate dementia.	For year 1-5: 10%, 9%, 8.1%, 7.3%, 6.6%; or transition to mild dementia.	10% per year up to 5 years or conversion to dementia.	10% per year up to 5 years or conversion to dementia.	10% per year above mortality disease status change. At 5-years on treatment.	10% per year until onset moderate dementia.
Indirect effect after discontinuation	Rate reverts to control after 5 years.	Rate reverts to control after 5 years.	n/s	Rate reverts to control after 5 years, accounting for better health due to treatment.	Symptom rates revert to what would have experienced with natural history; gains in actual symptom levels are maintained.	Natural Amyloid disease progression after discontinuation.	Treatment effect disappeared after moderate dementia progression.	Indirect effect on mortality (due to prolonged duration in MCI/dementia) remains.	Rate reverts to control after 5 years.	Rate reverts to untreated after 5 years.	Symptoms return to same level as control group.	Treatment effect extrapolated to 7 years and then maintained; gained progression delay remains over lifetime.
Other characteristics
Cycle/update time and timing of events	Annually.	Annually.	Annually.	2-year cycle, with half-cycle correction.	Symptom levels updated and AD dementia diagnostic criteria checked annually.	Disease equations evaluated every 6 months, other events (e.g., mortality) on continuous scale.	Discrete time until mild dementia and moderate dementia.	MCI, dementia, and mortality timings on continuous scale.	Annually.	Annually.	Monthly.	6-month interval.
Half-cycle correction of mean outcomesb	Yes	Yes	n/s	Yes	No	No	n/a	n/a	Yes	Yes	Yes	No
Half-cycle correction of proportions in each stateb,c	Yes	Yes	n/s	No	No	No	No	No	Yes	Yes	Yes	No
Assumptions	1) separate models for MCI and dementia assumed connected with same underlying progression speed; 2) ordered probit assumes proportional effects of predictors and no interactions were tested; 3) MCI dementia progression assumed independent from age; 4) cognition, function, and behavior are predictors for one another’s next state. 6) mortality life table includes dementia-related death.	1) Effect only apply when treated; 2) Conversion risk independent from age; 3) Costs, outcomes (QALYs), mortality rate dependent on age; 4) ordered probit assumed proportional effects of AD versus other/unspecified dementias and no interactions were tested; 5) mortality life table includes dementia-related death.	1) MCI was assumed to only convert to mild, mild could convert to moderate and severe, and moderate only to severe disease; 2) No backwards transitions were allowed.	1) effect lasts only while being treated, natural progression following discontinuation; 2) benefits of intervention are calculated in QALY terms, cost-effectiveness may not take into account cost savings or cost increase due to the intervention.	1) predementia exponential curves assumed 15 years between normal cognition and AD dementia diagnosis; 2) diagnostic thresholds for AD dementia by clinical diagnostic guidelines [McKhann, 2011] and calibrated based on mean symptom levels at diagnosis; 3) biomarker positivity only reflected in baseline symptom levels; 4) baseline patient characteristics APOE and AD family history not included because mixed evidence of independent effect on progression in biomarker positive patients; 5) symptomatic treatment use not considered in DMT arm, it was initiated in the standard of care arm at AD dementia diagnosis but did not influence disease progression.	1) Disease progression modeling was decoupled from disease staging; 2) The model relies on a noninterventional study to represent disease progression; 3) Modifying the components of the disease pathophysiology that are predictive of future disease progression in natural history is causative and their causal role is reversible.	CDR-SB lineal progression until moderate dementia.	1) dementia stage durations are not age-dependent, the age-dependency observed in literature is assumed to be present due to risk of dying due to competing risks. Stage durations for all age groups are taken from the youngest age group of Vermunt, 2019; 2) progression in the different stages is correlated within a certain individual (individual with fast progressing MCI will also have fast progressing dementia); 3) no transitions back to previous stages.	1) one singular model for MCI and three Alzheimer’s disease dementia states; 2) age-specific transitions; 3) mortality risk was age and health-state dependent and based on observed mortality in the NACC data as opposed a combination of population level mortality and dementia specific hazard ratios; 4) the model did not allow for reversion to less severe health states; 5) half cycle correction impacts first year of treatment but does not impact 5th year of treatment.	1) Ratchet imposed: no transition back to a less severe state. 2) Markov model which included MCI as a preliminary state before AD. 3) In AD analysis model is set to start at the AD mild dementia stage.	1) effect lasts only while being treated, natural progression following discontinuation; 2) treatment has no effect on mortality; 3) mild, moderate, and severe dementia defined only for the cross-model comparisons exercise and based on MMSE thresholds reported in the literature; 4) model did not incorporate utility estimates.	1) treatment effect extrapolated for both cognition and function beyond the initial 18 months as a linear function 2) costs and utilities modeled as function of time before Institutionalization, patients with predicted time < 6 months have cost/utility equal to those institutionalized. 3) institutionalized patients have fixed cost and utility while they remain in that health state. 4) assume treatment does not have a direct impact on mortality.

Abbreviations: AD, Alzheimer’s disease; ADNI, Alzheimer’s Disease Neuroimaging Initiative; bADL, basic activities of daily living; CDR-SB, Clinical Dementia Rating scale Sum of Boxes; CSF, cerebrospinal fluid; DAD, Disability Assessment Dementia; DICE, Discretely Integrated Condition Event; DMT, disease-modifying treatment; EU, European Union; FAQ, functional activities questionnaire; HR, hazard ratio; HRS, Health and Retirement Study; iADL, instrumental activities of daily living; IWG, International Working Group; KP, Kungsholmen project; MCI, mild cognitive impairment; MMSE, mini-mental state examination; MRI, magnetic resonance imaging; n/a, not applicable; n/s not stated; NACC, National Alzheimer’s Coordinating Center; NIA-AA, National Institute on Aging-Alzheimer’s Association; NINCDS-ADRDA, National Institute of Neurological and Communicative Disorders and Stroke and the Alzheimer’s Disease and Related Disorders Association; NPI, Neuropsychiatric Inventory; PET, positron emission tomography; QALY, quality-adjusted life year; RR, relative risk;SD, standard deviation; TICS, Telephone Interview for Cognitive Status; US, United States.

^aPrimary modeler to implement the benchmark scenario and generate the results.

^bAs applied for the benchmark cross-comparison results tables.

^cThat is, outcome reflecting mid-year estimate.

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