The DOI matches its Crossref record; 47 of the 48 references it cites were found in a registry or an index, and 1 are not checked yet; 4 of the 38 sources its claims cite were checked for support.
Duration of preclinical, prodromal, and dementia stages of Alzheimer's disease in relation to age, sex, and APOE genotype
Open accessAbstract
Introduction: We estimated the age‐specific duration of the preclinical, prodromal, and dementia stages of Alzheimer's disease (AD) and the influence of sex, setting, apolipoprotein E (APOE) genotype, and cerebrospinal fluid tau on disease duration. Methods: We performed multistate modeling in a combined sample of 6 cohorts (n = 3268) with death as the end stage and estimated the preclinical, prodromal, and dementia stage duration. Results: The overall AD duration varied between 24 years (age 60) and 15 years (age 80). For individuals presenting with preclinical AD, age 70, the estimated preclinical AD duration was 10 years, prodromal AD 4 years, and dementia 6 years. Male sex, clinical setting, APOE ε4 allele carriership, and abnormal cerebrospinal fluid tau were associated with a shorter duration, and these effects depended on disease stage. Discussion: Estimates of AD disease duration become more accurate if age, sex, setting, APOE, and cerebrospinal fluid tau are taken into account. This will be relevant for clinical practice and trial design.
Verified 2026-10-06 · 1 reference not checked yet
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20 Own result · 17 Not checked yet · 10 Own method · 7 Own interpretation · 1 Partly supported · accuracy not yet measured
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In the paper
“The study did not reveal significant sex differences in the duration of preclinical and prodromal AD stages.”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > DISCUSSION > Effect of sex
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“Figure 2A shows for those with preclinical AD a lower predicted overall disease duration at older age, which ranged from 24 years (95% CI, 22-25) at age 60 to 15 years (95% CI, 11-17) at age 80.”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > RESULTS > AD stage duration according to age, sex, and setting
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“There was no association of baseline abnormal t-tau with the duration of the dementia stages.”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > RESULTS > Tau effect
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“Figure 2C shows how the total predicted disease duration ranged from 12 to 25 years depending on APOE ε4 genotype, age and setting.”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > RESULTS > APOE effect
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“In females the moderate AD dementia stage duration was longer than in males (e.g. 2.1 years (95% CI, 1.1-3.2, p<0.0001 at age 70 in a clinical setting; Figure 2B, suppl. table B.3).”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > RESULTS > AD stage duration according to age, sex, and setting
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In the paper
“The estimation of total disease duration estimates were in some cases longer than the residual life expectancies of population data [46].”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > DISCUSSION > Duration and mortality
What the sources say
- Not checked yetcites [46] www.lifetable.de (2010-2012 USA).
hedged- Asserted: passes — The authors put it forward as true.
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In the paper
“The duration of preclinical AD at age 70 was shorter in a clinical setting (4 years [95% CI, 3-5]) than in a research setting (11 years [95% CI, 9-13]).”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > RESULTS > AD stage duration according to age, sex, and setting
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“In the model that included age, sex and setting, all transition rates to subsequent disease were significantly influenced by age, except mortality in the preclinical AD stage and progression from prodromal AD to mild AD dementia”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > RESULTS > Transition rates
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In the paper
“Progression to at least one consecutive stage was apparent in 981 (32% of 3,034) participants.”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > RESULTS
plainSingle case- Asserted: passes — The authors put it forward as true.
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In the paper
“Individuals with preclinical AD and abnormal CSF t-tau showed a trend for an increased progression rate from preclinical to prodromal AD (HR=1.49 [95% CI, 0.95-2.35]).”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > RESULTS > Tau effect
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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- Probably not a substantial claim. 16
- It may state two separate claims as one. 28
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Attempts to quantify the duration of AD should be age-specific, because age imposes the greatest risk for both dementia and mortality, and take into account APOE genotype, sex, and cerebrospinal fluid (CSF) tau levels [4, 6, 10-12].”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > INTRODUCTION
What the sources say
- Partly supportedcites [4] Jansen WJ,, Prevalence of cerebral amyloid pathology in persons without dementia: a meta-analysis. JAMA, 2015 313(19): p. 1924– 38. 25988462 PMC4486209 sourceExperimental — accuracy not yet measured
The Results (Comparison With Prevalence of AD-Type Dementia; page unavailable) compare age- and APOE genotype–specific amyloid prevalence with dementia estimates, supporting the relevance of those factors to estimates of AD timing. The Methods (Statistical Analysis; page unavailable) include sex, but the Discussion reports no association between sex and amyloid positivity. The paper does not recommend accounting for CSF tau levels when estimating AD duration or establish the stated mortality rationale. (LLM, conf=0.84)
- Partly supportedcites [6] Jack CR Jr.,, NIA-AA Research Framework: Toward a biological definition of Alzheimer's disease. Alzheimers Dement, 2018 14(4): p. 535– 562. 29653606 PMC5958625 sourceExperimental — accuracy not yet measured
Section 6 reports age-specific prevalence of AD dementia, and section 15 notes that death rates rise with age during AD’s long preclinical period. Sections 9.3 and 12 discuss CSF tau as a biomarker and APOE ε4 as a risk allele. These passages support considering age, mortality, tau, and genetic risk, but they do not recommend that duration estimates be age-specific or account for APOE genotype, sex, and CSF tau levels as stated. (LLM, conf=0.75)
- Partly supportedcites [10] Neu SC,, Apolipoprotein E Genotype and Sex Risk Factors for Alzheimer Disease: A Meta-analysis. JAMA Neurol, 2017 74(10): p. 1178– 1189. 28846757 PMC5759346 sourceExperimental — accuracy not yet measured
The Methods and Discussion examine how Alzheimer’s disease risk varies by age, APOE genotype, and sex, supporting consideration of those factors. The paper does not assess disease duration or CSF tau levels, and it does not make the claimed recommendation about duration estimates. (LLM, conf=0.85)
- Not checked yetcites [11] Lim YY,, Association of beta-Amyloid and Apolipoprotein E epsilon4 With Memory Decline in Preclinical Alzheimer Disease. JAMA Neurol, 2018 75(4): p. 488– 494. 29356823 PMC5933393
- Partly supportedcites [12] Vos SJ,, Preclinical Alzheimer's disease and its outcome: a longitudinal cohort study. Lancet Neurol, 2013 12(10): p. 957– 65. 24012374 PMC3904678 sourceExperimental — accuracy not yet measured
The Methods (Statistical analyses; page unavailable) adjust progression analyses for age, gender, and APOE genotype, while the Introduction identifies CSF tau as a marker used to define preclinical AD stages. The Discussion reports that preclinical AD was more common in older participants and APOE-ε4 carriers, but neither age nor APOE genotype predicted the rate of decline in its subgroup analyses. The paper does not recommend age-specific estimates of AD duration or say that duration estimates should account for all four factors. (LLM, conf=0.84)
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. It may be too vague to check against evidence. It may state two separate claims as one.
- Partly supported
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The estimated preclinical AD stage was shortened by around 3 years and the prodromal AD stage by around 2.5 years (Table 3).”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > RESULTS > Tau effect
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In prodromal AD, abnormal tau associated with a decreased reversion rate to preclinical AD stage (HR=0.41 [95% CI, 0.23-0.71]) and increased progression rate to the mild AD dementia stage (HR=1.91 [95% CI, 1.48-2.48]).”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > RESULTS > Tau effect
plaincorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Compared to data collected in a research setting, data from clinical settings was associated with a higher progression rate (HR=4.40 [95% CI, 2.80-6.94]) and reversion rate (HR=1.98 [95% CI, 1.15-3.39]) between preclinical and prodromal AD.”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > RESULTS > Transition rates
plaincorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Additionally, in the clinical setting the progression rates from the prodromal AD to the mild AD dementia stage (HR=1.48 [95% CI, 1.34-1.92]) and from the mild AD to the moderate AD dementia stage (HR=1.41 [95% CI,1.16-1.72]) were higher.”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > RESULTS > Transition rates
plaincorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Females had a higher progression rate from mild AD to moderate AD dementia, compared to males (HR=1.24 [95% CI, 1.04-1.47]), while their mortality risk in moderate AD dementia was lower (HR=0.60 [95% CI, 0.46-0.80]).”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > RESULTS > Transition rates
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The predicted total disease duration, based on the model with age, for an individual with preclinical AD at age 70 was 20 years (95% CI, 17-21), consisting of a preclinical stage of 10 years (95% CI, 8-11), followed by a prodromal stage of 4 years (95% CI, 3-5), mild AD dementia for 3 years (95% CI, 2-3), and moderate AD dementia for 3 years (95% CI, 2-3, Table 2).”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > RESULTS > AD stage duration according to age, sex, and setting
plain- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In the clinical setting, for individuals with prodromal AD, the stage duration of prodromal AD was also shorter, and while the dementia stage duration for these individuals was equal between settings, more time was spent in the moderate AD stage (Suppl. table B.7a and b).”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > RESULTS > AD stage duration according to age, sex, and setting
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Depending on age, sex, APOE genotype, baseline CSF t-tau and setting, the total disease duration varied between 12 and 25 years, the preclinical stage between 2 and 15, the prodromal stage between 3 to 7, mild AD dementia stage between 2 and 6 and moderate AD dementia stage between 1 and 7 years.”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > DISCUSSION
plaincorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“When compared to a non-carrier, an APOE ε4 carrier aged 70 in the clinical setting had a 1.6 years (95% CI, 0.4-3.3; p=0.0295) shorter estimated preclinical AD stage duration, and 1.1 years (95% CI, 0.3-2.1; p=0.0110) shorter prodromal AD stage duration, but 1.0 year (95% CI, 0.3-1.8; p=0.0050) longer mild dementia stage duration (suppl. table B.4).”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > RESULTS > APOE effect
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The estimated total duration with starting stage preclinical AD ranged in the clinical setting 19 years (95% CI, 17-20) at age 60 to 11 years (95% CI, 10-12) at age 80 and in the research setting from 26 years (95% CI, 23-28) at age 60 to 15 years (95% CI, 12-17) at age 80.”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > RESULTS > AD stage duration according to age, sex, and setting
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“APOE ε4 carriers had, compared to non-carriers, an increased rate of progression from the preclinical AD to prodromal AD stage (HR=1.63 [95% CI, 1.11-2.41]) and from the prodromal AD to mild AD dementia stage (HR=1.50 [95% CI, 1.18-1.90]), and a trend for slower decline from the mild to the moderate AD dementia stage (HR 0.77 [95% CI, 0.60-1.00]).”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > RESULTS > APOE effect
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Unlike previous studies, no effect of tau on mortality and duration of the AD dementia stage were found, which may be explained by dichotomization of CSF t-tau in our analysis [16, 17].”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > DISCUSSION > Effect of tau
What the sources say
- Not checked yetcites [16] Rhodius-Meester HFM,, Disease-related determinants are associated with mortality in dementia due to Alzheimer's disease. Alzheimers Res Ther, 2018 10(1): p. 23. 29458426 PMC5819199
- Not checked yetcites [17] Degerman Gunnarsson M,, High tau levels in cerebrospinal fluid predict nursing home placement and rapid progression in Alzheimer's disease. Alzheimers Res Ther, 2016 8(1): p. 22. 27263933 PMC4893835
hedged- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“For example, the residual life expectancy at age 80 was reported to be 8-10 years in the USA and Australia (data from 2010-2012), while in our study this ranged from 4 years for those with moderate AD to 15 years for individuals with preclinical AD.”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > DISCUSSION > Duration and mortality
What the sources say
- Not checked yetcites [46] www.lifetable.de (2010-2012 USA).
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Accumulation of amyloid in the brain is believed to be the first sign of the disease and can precede a clinical diagnosis of dementia by up to 20 years [1, 4, 5].”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > INTRODUCTION
What the sources say
- Not checked yetcites [1] Winblad B,, Defeating Alzheimer's disease and other dementias: a priority for European science and society. Lancet Neurol, 2016 15(5): p. 455– 532. 26987701 source
- Not checked yetcites [4] Jansen WJ,, Prevalence of cerebral amyloid pathology in persons without dementia: a meta-analysis. JAMA, 2015 313(19): p. 1924– 38. 25988462 PMC4486209 source
- Not checked yetcites [5] Jack CR Jr.,, Tracking pathophysiological processes in Alzheimer's disease: an updated hypothetical model of dynamic biomarkers. Lancet Neurol, 2013 12(2): p. 207– 16. 23332364 PMC3622225 source
plainconditional- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Age had the strongest effect on the duration of the preclinical and dementia stages, which could be explained by higher progression and mortality rates.”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > DISCUSSION > Effect of age
hedgedconditional- Asserted: passes — The authors put it forward as true.
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- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The dementia stage duration was longer in women, which was driven by lower mortality in this group.”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > DISCUSSION > Effect of sex
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Varying the mortality assumptions for unknown mortality dates of those who died, did not change the results.”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > RESULTS > Sensitivity analyses
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“The effects of setting on disease progression are consistent with other AD studies [40, 41].”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > DISCUSSION > Effect of setting
What the sources say
- Not checked yetcites [40] Qian J,, APOE-related risk of mild cognitive impairment and dementia for prevention trials: An analysis of four cohorts. PLoS Med, 2017 14(3): p. e1002254. 28323826 PMC5360223
- Not checked yetcites [41] Snitz BE,, Risk of progression from subjective cognitive decline to mild cognitive impairment: The role of study setting. Alzheimers Dement, 2018 14(6): p. 734– 742. 29352855 PMC5994356
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“While the prodromal stage was shorter in APOE ε4 carriers, the dementia stage was longer which would imply that the total symptomatic disease duration is similar, but differently divided over the stages.”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > DISCUSSION > Effect of APOE genotype
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The patients with prodromal AD and increased CSF t-tau levels tended to convert sooner to AD dementia [19, 20].”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > INTRODUCTION
What the sources say
- Not checked yetcites [19] van Rossum IA,, Injury markers predict time to dementia in subjects with MCI and amyloid pathology. Neurology, 2012 79(17): p. 1809– 16. 23019259 PMC3475623 source
- Not checked yetcites [20] Buchhave P,, Cerebrospinal fluid levels of beta-amyloid 1-42, but not of tau, are fully changed already 5 to 10 years before the onset of Alzheimer dementia. Arch Gen Psychiatry, 2012 69(1): p. 98– 106. 22213792 source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“Previous studies on the length of the AD dementia stage reported a duration of 3 to 10 years [14, 15].”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > INTRODUCTION
What the sources say
- Not checked yetcites [14] Brodaty H, Seeher K, and Gibson L, Dementia time to death: a systematic literature review on survival time and years of life lost in people with dementia. Int Psychogeriatr, 2012 24(7): p. 1034– 45. 22325331 source
- Not checked yetcites [15] Wattmo C, Londos E, and Minthon L, Risk factors that affect life expectancy in Alzheimer's disease: a 15-year follow-up. Dement Geriatr Cogn Disord, 2014 38(5-6): p. 286– 99. 24992891
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“Younger age, female sex and lower CSF total tau (t-tau) were found to be associated with a longer duration of the AD dementia stage, while the effect of APOE genotype was equivocal [14-17].”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > INTRODUCTION
What the sources say
- Not checked yetcites [14] Brodaty H, Seeher K, and Gibson L, Dementia time to death: a systematic literature review on survival time and years of life lost in people with dementia. Int Psychogeriatr, 2012 24(7): p. 1034– 45. 22325331 source
- Not checked yetcites [15] Wattmo C, Londos E, and Minthon L, Risk factors that affect life expectancy in Alzheimer's disease: a 15-year follow-up. Dement Geriatr Cogn Disord, 2014 38(5-6): p. 286– 99. 24992891
- Not checked yetcites [16] Rhodius-Meester HFM,, Disease-related determinants are associated with mortality in dementia due to Alzheimer's disease. Alzheimers Res Ther, 2018 10(1): p. 23. 29458426 PMC5819199
- Not checked yetcites [17] Degerman Gunnarsson M,, High tau levels in cerebrospinal fluid predict nursing home placement and rapid progression in Alzheimer's disease. Alzheimers Res Ther, 2016 8(1): p. 22. 27263933 PMC4893835
plaincorrelational- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“For example, exclusion of ε4 carriers during a trial, what happened in the high-dose group of the BAN2401 trial, may affect rate of progression and possibly the power of the study [45].”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > DISCUSSION > Effect of APOE genotype
What the sources say
- Not checked yetcites [45] https://www.alzforum.org/news/conference-coverage/ban2401-removes-brain-amyloid-possibly-slows-cognitive-decline 20 2 2019].
hedgedconditional- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“The median duration of prodromal AD was three years in a pooled memory clinic cohort study, but no age-specific estimates were provided and mortality was not taken into account [18].”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > INTRODUCTION
What the sources say
- Not checked yetcites [18] Vos SJ,, Prevalence and prognosis of Alzheimer's disease at the mild cognitive impairment stage. Brain, 2015 138(Pt 5): p. 1327– 38. 25693589 PMC5013930 source
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The shorter age-specific duration of the preclinical stage in APOE ε4 carriers is consistent with the observed earlier onset of dementia due to AD in epidemiological studies and the faster cognitive decline of APOE ε4 carriers with preclinical AD in research studies [11, 42-44].”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > DISCUSSION > Effect of APOE genotype
What the sources say
- Not checked yetcites [11] Lim YY,, Association of beta-Amyloid and Apolipoprotein E epsilon4 With Memory Decline in Preclinical Alzheimer Disease. JAMA Neurol, 2018 75(4): p. 488– 494. 29356823 PMC5933393
- Not checked yetcites [42] Roberts RO,, Prevalence and Outcomes of Amyloid Positivity Among Persons Without Dementia in a Longitudinal, Population-Based Setting. JAMA Neurol, 2018. PMC6142936 29710225 source
- Not checked yetcites [43] van der Lee SJ,, The effect of APOE and other common genetic variants on the onset of Alzheimer's disease and dementia: a community-based cohort study. Lancet Neurol, 2018 17(5): p. 434– 444. 29555425
- Not checked yetcites [44] Mormino EC,, Amyloid and APOE epsilon4 interact to influence short-term decline in preclinical Alzheimer disease. Neurology, 2014 82(20): p. 1760– 7. 24748674 PMC4035706
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“The duration of the preclinical AD stage has been estimated in combination with the prodromal AD stage, which was 17 years, based on extrapolations of change in positron emission tomography (PET) amyloid load over time [21].”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > INTRODUCTION
What the sources say
- Not checked yetcites [21] Villemagne VL,, Amyloid beta deposition, neurodegeneration, and cognitive decline in sporadic Alzheimer’s disease: a prospective cohort study. Lancet Neurol, 2013 12. 23477989 source
hedged- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The presence of increased CSF t-tau was associated with a shorter pre-dementia disease duration, which confirms that increased tau is associated with faster disease progression.”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > DISCUSSION > Effect of tau
boostedcorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“When all variables were combined in one model, most estimates remained unchanged.”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > RESULTS > Sensitivity analyses
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“In the additional analysis of the same models in the subset of individuals with all covariates (n=1518, see Suppl. Table B.8), the effects were similar.”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > RESULTS > Sensitivity analyses
plainn = 1,518- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Setting is also important, as progression from MCI to dementia was longer in research settings than in clinical settings [13].”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > INTRODUCTION
What the sources say
- Not checked yetcites [13] Farias ST,, Progression of mild cognitive impairment to dementia in clinic- vs community-based cohorts. Arch Neurol, 2009 66(9): p. 1151– 7. 19752306 PMC2863139
plaincorrelational- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Male sex, clinical setting, APOE ε4 genotype and abnormal CSF tau were associated with a shorter duration and these effects depended on disease stage.”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > Abstract > Results
plaincorrelational- Asserted: passes — The authors put it forward as true.
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What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“A strength of the study is the large sample of participants with amyloid accumulation.”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > DISCUSSION > Strengths and limitations
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Finally, our sample is not representative of the general population, but may be representative of the patients who physicians need to inform, and volunteers that participate in clinical trials.”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > DISCUSSION > Strengths and limitations
hedged- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“Additionally, we used the old criteria for the preclinical AD definition, while the recent research criteria also require tau positivity [8].”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > DISCUSSION > Strengths and limitations
What the sources say
- Not checked yetcites [8] Sperling RA,, Toward defining the preclinical stages of Alzheimer’s disease: recommendations from the National Institute on Aging-Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer’s disease. Alzheimers Dement, 2011 7. PMC3220946 21514248 source
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“As such, the sample consisted of over 3000 individuals, still not all the effects were estimable.”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > DISCUSSION > Strengths and limitations
plainn = 3,000- Asserted: passes — The authors put it forward as true.
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- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“The multi-state model approach is another strength, because it enabled the incorporation of multiple clinical stages, including fluctuations between stage, and the mortality risk in a data driven manner.”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > DISCUSSION > Strengths and limitations
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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Probably not a substantial claim.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Another limitation was that amyloid status and APOE genotype were unknown for AD-type dementia patients of the ICTUS study, but the sensitivity analysis without the ICTUS, yielded very similar results.”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > DISCUSSION > Strengths and limitations
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper relies on this without support.
It is unclear how long individuals with amyloid pathology spend in each Alzheimer's disease stage.
“but it is unclear how long individuals with amyloid pathology spend in each stage.”
The authors state this as an assumption.
Progression risk is independent of the time already spent in a stage.
“underlying assumption that progression risk is independent on the previous time spend in a stage”
The paper relies on this without support.
A better understanding of the stage-specific duration of Alzheimer's disease is needed to inform patients, caregivers, and clinicians.
“A better understanding of the stage-specific duration of AD is needed to inform patients, caregivers, and clinicians.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“Longitudinal studies of cognitive function and CSF and neuroimaging biomarker changes in ADAD and LOAD have identified a significant preclinical phase of disease preceding onset of clinical symptoms by at least 10-20 years”
From Alzheimer Disease: An Update on Pathobiology and Treatment Strategies (2019) · cites this paper as Vermunt et al., 2019
In the citing paper
“Though this represents an intermediate phase of clinical disease, this is actually an advanced stage of the biological disease when considering that pathology accumulates in the AD brain 15-20 years prior to onset of clinical symptoms (Vermunt et al., 2019).”
From Alzheimer Disease: An Update on Pathobiology and Treatment Strategies (2019) · cites this paper as Vermunt et al., 2019
In the citing paper
“Aberrant Aβ deposition begins over a decade before the onset of clinical symptoms and spreads diffusely throughout the cerebral cortex [16, 17].”
From Systems-based proteomics to resolve the biology of Alzheimer’s disease beyond amyloid and tau (2021) · cites this paper as [17]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > DISCUSSION
“Depending on age, sex, APOE genotype, baseline CSF t-tau and setting, the total disease duration varied between 12 and 25 years”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > RESULTS > AD stage duration according to age, sex, and setting
“The estimated total duration with starting stage preclinical AD ranged in the clinical setting 19 years (95% CI, 17-20) at age 60 to 11 years (95% CI, 10-12) at age 80 and in the research setting from 26 years (95% CI, 23-28) at age 60 to 15 years (95% CI, 12-17) at age 80.”
Citations
Cites
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“Prodromal AD was in this study defined by amyloid accumulation and a diagnosis of mild cognitive impairment, amnestic and nonamnestic [9,32,33].”
BackgroundMild Cognitive Impairment: Clinical Characterization and Outcome
Petersen, R. C., Smith, G. E., Waring, S. C., Ivnik, R. J., Tangalos, E. G., & Kokmen, E. (1999) · Archives of Neurology · doi:10.1001/archneur.56.3.303 · Cited by 8,980
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“Prodromal AD was in this study defined by amyloid accumulation and a diagnosis of mild cognitive impairment, amnestic and nonamnestic [9,32,33].”
BackgroundSelf-citationJack, C. R., Knopman, D. S., Jagust, W. J., Petersen, R. C., Weiner, M. W., Aisen, P. S., Shaw, L. M., Vemuri, P., Wiste, H. J., Weigand, S. D., et al. (2013) · The Lancet Neurology · doi:10.1016/s1474-4422(12)70291-0 · Cited by 4,396
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Self-citationAlbert, M., DeKosky, S. T., Dickson, D. W., Dubois, B., Feldman, H., Fox, N. C., Gamst, A. C., Holtzman, D. M., Jagust, W. J., Petersen, R. C., et al. (2013) · FOCUS The Journal of Lifelong Learning in Psychiatry · doi:10.1176/appi.focus.11.1.96 · Cited by 2,643
Research works printed but not linked: 1
- TFagan GStrobelhttps://www.alzforum.org/news/conference‐coverage/ban2401‐removes‐brain‐amyloid‐possibly‐slows‐cognitive‐declineAccessed February 20 2019.
Cited by
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Items 301–400 of 575
Lin, Y., Luo, X., Wang, F., Cai, H., Lin, Y., Kang, D., & Fang, W. (2025) · Biology of Sex Differences · doi:10.1186/s13293-025-00684-w · Cited by 7
“…anxiety-phenotype and therapeutic effect of metformin in the aged apoE-TR mice Yingbin Lin 1* , Xinqun Luo 1 , Fangyu Wang 1 , Huange Cai 2 , Yuanxiang Lin 1 , Dezhi Kang 1 and Wenhua Fang 1* Background Apolipoprotein E4 ( APOE4 ) is a risk factor for developing Alzheimer’s disease (AD) [1].”
The effect of sleep disturbances on the incidence of dementia for varying lag times
Alders, P., Kok, A. A. L., van Zutphen, E. M., Claassen, J. A. H. R., & Deeg, D. J. H. (2025) · The Journal of Prevention of Alzheimer s Disease · doi:10.1016/j.tjpad.2024.100024 · Cited by 6
Akkol, E. K., Karatoprak, G. Ş., Dumlupınar, B., Açıkara, Ö. B., Arıcı, R., Yücel, Ç., Aynal, L. C., & Sobarzo‐Sánchez, E. (2025) · Molecules · doi:10.3390/molecules30091982 · Cited by 8
Contreras, A., Jiménez‐Herrera, R., Djebari, S., Navarro‐López, J. D., & Jiménez‐Díaz, L. (2025) · Biology of Sex Differences · doi:10.1186/s13293-025-00697-5 · Cited by 7
“That age is considered a good representation of the pre-clinical stages of AD, which occur decades before disease onset [91].”
Systemic medications and dementia risk: a systematic umbrella review
Belessiotis‐Richards, C., Hayes, J., Yap, Y. F., Talwar, S., Eskinazi, M., Li, W., Ward, H., Letrondo, P. A., Morelli‐Batters, M., Bruun, A., et al. (2025) · Molecular Psychiatry · doi:10.1038/s41380-025-03129-3 · Cited by 9
Cannabidiol improves learning and memory deficits and alleviates anxiety in 12-month-old SAMP8 mice
Goodland, M. N., Banerjee, S., Niehoff, M. L., Young, B. J., Macarthur, H., Butler, A. A., Morley, J. E., & Farr, S. A. (2025) · PLoS ONE · doi:10.1371/journal.pone.0296586 · Cited by 10
“CBD has been known to inhibit A β induce neuro inflammation one of the neuropathologies that underlie the development of Alzheimer’s disease (AD) [16], progressive neurodegenerative disorder that causes cognitive impairment, culminating in dementia and eventually death [17].”
Ajith, T. A., & Sreejith, J. K. (2025) · Nutritional Neuroscience · doi:10.1080/1028415x.2025.2567429 · Cited by 7
“Despite differences with environmental and genetic-related factors, a preclinical asymptomatic period lasting an average of 10 years and a prodromal stage, in the presence of a positive biomarker, lasting an average of 4 years were observed in elder AD patients [1].”
Role of proline‐rich tyrosine kinase 2 (Pyk2) in the pathogenesis of Alzheimer's disease
Kumar, R. K., Tiwari, V., & Dey, S. (2021) · European Journal of Neuroscience · doi:10.1111/ejn.15569 · Cited by 9
“AD is associated with a progressive disability during the course of disease and eventually leads to death within 5 to 12 years of onset of symptoms (Vermunt et al., 2019).”
BackgroundPredicting cognitive decline: Which is more useful, baseline amyloid levels or longitudinal change?
Chen, G., McKay, N. S., Gordon, B. A., Liu, J., Joseph‐Mathurin, N., Schindler, S. E., Hassenstab, J. J., Aschenbrenner, A. J., Wáng, Q., Schultz, S. A., et al. (2023) · NeuroImage Clinical · doi:10.1016/j.nicl.2023.103551 · Cited by 7
“Previous research has highlighted that AD has a long preclinical phase lasting 10–20 years (Vermunt et al., 2019).”
Handels, R. L. H., Herring, W. L., Kamgar, F., Aye, S., Tate, A., Green, C., Gustavsson, A., Wimo, A. B., Winblad, B. G., Sköldunger, A., et al. (2024) · Value in Health · doi:10.1016/j.jval.2024.09.006 · Cited by 7
Self-citationThe Janus-like Association between Proton Pump Inhibitors and Dementia
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Krankheitsmodifizierende Therapieansätze bei Alzheimer-Krankheit
Frölich, L., & Hausner, L. (2021) · Der Nervenarzt · doi:10.1007/s00115-021-01222-w · Cited by 7
An insight into Alzheimer’s disease and its on-setting novel genes
Vigneswaran, J., Muthukumar, S. A., Shafras, M., & Pant, G. (2021) · The Egyptian Journal of Neurology Psychiatry and Neurosurgery · doi:10.1186/s41983-021-00420-2 · Cited by 7
Guo, Q., Wu, G., Huang, F., Wei, Z. C., Wang, J., Zhang, B., Liu, R., Yang, Y., Wang, X., & Li, H. (2022) · Aging · doi:10.18632/aging.204336 · Cited by 7
Qiu, T., Zeng, Q., Zhang, Y., Luo, X., Xu, X., Li, X., Shen, Z., Li, K., Wang, C., Huang, P., et al. (2022) · European Journal of Neuroscience · doi:10.1111/ejn.15860 · Cited by 7
Huang, Y., Xie, X.-X., Yang, J., Sun, X., Niu, X.-Y., Yang, C., Li, L., Zhang, L., Wang, D., Liu, C.-Y., et al. (2023) · Cell Reports · doi:10.1016/j.celrep.2023.112624 · Cited by 9
Kang, D. W., Wang, S., Um, Y. H., Kim, S., Kim, T., Kim, D., Lee, C. U., & Lim, H. K. (2023) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2023.1234086 · Cited by 7
“Given that the transition from MCI to AD takes 4–5 years (Vermunt et al., 2019), it is important to assess the impact of long-term changes in white matter microstructural integrity on changes in cognitive function and the risk of transition from MCI to AD.”
BackgroundInfluence of cerebral blood flow on volumetric loss related to Alzheimer’s disease
Agnollitto, M. I. S. S., Leoni, R. F., Foss, M. P., Palaretti, J., Cayres, M., Pansarim, V., Nather, J. C., Zotin, M. C. Z., Ferrioli, E., Lima, N. K. D. C., et al. (2023) · Dementia & Neuropsychologia · doi:10.1590/1980-5764-dn-2023-0004 · Cited by 7
Hodgson, L. M., Li, Y., Iturria‐Medina, Y., Stratton, J. A., Wolf, G., Krishnaswamy, S., Bennett, D. A., & Bzdok, D. (2024) · Communications Biology · doi:10.1038/s42003-024-06273-8 · Cited by 7
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Mood Alterations in the Prodromal Phase of Sporadic Creutzfeldt-Jakob Disease
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“Other activities that may be especially sensitive to change over The AD course is believed to last 15 years or more before apparent clinical symptoms emerge, 26 and detecting changes in the preclinical stage is not easy with the standard tests that have been in use for decades.”
The Diagnostic and Therapeutic Potential of Oligonucleotide Aptamers in Alzheimer’s Disease
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“The time required for full-blown AD symptoms is a factor of age, genetics, gender, educational level, etc. [8].”
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“…its progression [48], and acknowledging the extended duration, often exceeding a decade, required for dementia to manifest in preclinical stages [49], a PUD diagnosis in individuals in their 60s and above, combined with a high concurrent H. pylori infection prevalence, could significantly…”
Rogers, B. (2025) · Alzheimer s & Dementia · doi:10.1002/alz.14564 · Cited by 6
“21 Early-onsetAD(EOAD)typicallypresentsinindividualsunder the age of 65 and has distinct patterns of progression in comparison to late-onset AD (LOAD), which is more common in older adults.”
Omega-3 fatty acids, brain health and the menopause
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Novel mathematical model based on cellular automata for study of Alzheimer’s disease progress
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“Amyloid-β (Aβ) plaque and neurofibrillary tangles (NFT) of hyperphosphorylated tau are two main pathologies factors of AD (Weller and Budson 2018).”
BackgroundCNN-SVM for prediction Alzheimer disease in early step
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“The disease affects 23% of the population after 80 years [1-7].”
BackgroundWang, S., Fang, X., Wen, X., Yang, C., Yang, Y., & Zhang, T. (2023) · Frontiers in Genetics · doi:10.3389/fgene.2023.1190863 · Cited by 6
“Although most patients with AD experience the first symptom in their mid-60s, previous studies have indicated that changes in the molecular levels occur at a much earlier stage [17-18].”
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“One potential explanation for the conflicting results regarding the association between late-life obesity and dementia risk is that the clinical diagnosis of dementia often comes after a lengthy preclinical and prodromal phase that can span several decades [41, 45].”
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“BCHE-K may join APOE4 allele frequency, age, and sex as a foundational component of predictive modeling for early AD phenotypes [93, 94].”
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“The presence of an ε 4 allele has also been found to increase the rate of transition between the preclinical and symptomatic stages of AD (Vermunt et al., 2019) and the presence of an ε 4 allele has been found to be associated with higher amyloid lesion burden (Pletnikova et al., 2018).”
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“A considerable time window exists before symptoms of cognitive impairment appear, during which time lifestyle behaviors and other risk factors are modi fi able [2, 3].”
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“Indeed, since neuropathological changes likely occur 15 to 25 years before any clinical diagnosis can be reached [10, 14], confirming the sequence and timing of the associated neuropathological changes would require a follow-up of more than 20 years before diagnosis of clinical dementia which is only possible in popul…”
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“However, it might take at least 10-20 years from the presence of neuropathological hallmarks to the onset of clinical symptoms (4), leading to a huge challenge in its early diagnosis and prevention.”
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“Preclinical and prodromal AD respectively lasts on average for 10 and 4 years (Vermunt et al., 2019) before becoming dementia.”
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“Alzheimer’s Disease (AD) is a neurodegenerative disease characterized by memory and cognitive impairment, which most commonly occurs in old age (Vermunt et al., 2019).”
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“12 Diet has emerged as a promising target for dementia prevention.”
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“A large number of studies have indicated that the pathological development of AD preceded the appearance of clinical symptoms by several decades [27].”
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“Similarly, a female patient who develops dementia at 65 years of age may experience moderate-to-severe dementia for approximately 6 years [4].”
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“Indeed, amyloid deposition can precede the clinical symptoms of AD by more than 10 years [29], necessitating long-term follow-up with neuropsychological tools sensitive to cognitive changes in preclinical or prodromal AD, and possible individual assessment of AD risk including genetic risk profiles…”
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Kärkkäinen, V., Saari, T. T., Hannonen, S., Rusanen, M., Lehtola, J.-M., Uusitalo, H. M. T., Leinonen, V., Thiede, B., Kaarniranta, K., Koivisto, A. M., et al. (2025) · Journal of Alzheimer s Disease · doi:10.1177/13872877251326868 · Cited by 4
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“…medication on memory and cognitive function warrant further investigation with personalized assessments of Alzheimer’s risk, including genetic profiling, especially since plasma amyloid biomarkers may yield inconclusive results in individuals undergoing sacubitril/ valsartan therapy [65–67].”
Cai, Y., Schrack, J. A., Agrawal, Y., Armstrong, N. M., Wanigatunga, A. A., Kitner‐Triolo, M. H., Moghekar, A., Ferrucci, L., Simonsick, E. M., Resnick, S. M., et al. (2023) · Aging & Mental Health · doi:10.1080/13607863.2023.2227118 · Cited by 4
“This preclinical stage can take up to 20 years prior to a dementia diagnosis (Kessler & Üstün, 2004; Kessler et al., 2004; Vermunt et al., 2019).”
Wang, T., Zhang, W., Maclin, J. M. A., Xu, H. J., Hong, B., Yan, F., Liu, Y., He, H., Liang, H., Li, C., et al. (2024) · Journal of Alzheimer s Disease · doi:10.3233/jad-231446 · Cited by 4
“Clinicians and neurologists must recognize AD symptoms to diagnose it accurately and promptly [4].”
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“Early intervention can delay disease progression or alter the trajectory toward dementia [9,14,15].”
The financial consequences of undiagnosed memory disorders
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“…created by early stage ADRD is compounded by the challenges of detecting and diagnosing mild cognitive impairment (Sabbagh et al., 2020) and the years-long time span of the prodromal stage, when mild symptoms may be manifesting but diagnosis may not yet be possible (Vermunt et al., 2019).”
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“Clinical manifestations can include mild cognitive impairment (MCI), subjective cognitive impairment (SCI), and varying degrees of AD dementia [18–22].”
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“The prolonged progression of AD involves three clinical stages, based on the occurrence and severity of cognitive deficits [21].”
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“Despite the presence of detectable brain pathology, many individuals with AD will remain asymptomatic for decades prior to the emergence of clinically measurable cognitive impairment [47, 48].”
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“Dementia is a slowly progressing disease with a long preclinical stage [41], thus, one could argue that loneliness might be a preclinical symptom of dementia.”
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“Unlike rapidly progressive dementias (RPDs) that are fatal within a few months to years after its onset (Geschwind et al., 2007), AD is a slowly progressive dementia that leads to inevitable death between 4 and 20 years after diagnosis in patients above 60 years of age (Vermunt et al., 2019).”
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Metadata
- Authors
- Vermunt, L., Sikkes, S. A. M., van den Hout, A., Handels, R., Bos, I., van der Flier, W. M., Kern, S., Ousset, P., Maruff, P., Skoog, I., Verhey, F. R. J., Freund‐Levi, Y., Tsolaki, M., Wallin, Å. K., Olde Rikkert, M., Soininen, H., Spiru, L., Zetterberg, H., Blennow, K., Scheltens, P., Muniz‐Terrera, G., Visser, P. J., Initiative, F. T. A. D. N., AIBL Research Group, & groups, I. S.
- Affiliations
- Amsterdam Neuroscience (NL)
- Harvard University (US)
- Department of Statistical Science University College London London UK
- Maastricht University (NL)
- Department of Neurology Alzheimer Center Amsterdam Amsterdam Neuroscience Amsterdam UMC Vrije Universiteit Amsterdam Amsterdam The Netherlands
- University of Gothenburg (SE)
- Inserm (FR)
- The University of Melbourne (AU)
- Karolinska University Hospital (SE)
- Aristotle University of Thessaloniki (GR)
- Lund University (SE)
- Department of Geriatric Medicine Radboudumc Alzheimer Centre Radboud University Medical Center Nijmegen The Netherlands
- University of Eastern Finland (FI)
- Carol Davila University of Medicine and Pharmacy (RO)
- Sahlgrenska University Hospital (SE)
- Centre for Dementia Prevention University of Edinburgh Edinburgh UK
- Corresponding author
- Vermunt, Lisa
- ORCID
- Venue
- Alzheimer's & Dementia
- Publisher
- Wiley
- Published
- 2019-06
- Volume
- 15
- Issue
- 7
- Pages
- 888-898
- ISSN
- 1552-5260 (ISSN-L)
- 1552-5279
- PMC
- PMC6646097
- OpenAlex
- W2947634966
- Semantic Scholar
- a7cc914d460367dcba0fdb7e9290bc681d8a3b4a
- Cited by
- 570
- References
- 48
- Citations by year
- 2026: 70 · 2025: 100 · 2024: 115 · 2023: 81 · 2022: 94 · 2021: 68 · 2020: 37 · 2019: 2
- FWCI
- 39.95
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Alzheimer s & Dementia (publishedVersion)
- PubMed (publishedVersion)
- Research Publications (Maastricht University) (publishedVersion, other-oa)
- Amsterdam UMC (VU Amsterdam) - Institutional Repository (publishedVersion)
- PubMed Central (acceptedVersion)
- Research at the University of Copenhagen (University of Copenhagen) (acceptedVersion, other-oa)
- Archive ouverte UNIGE (University of Geneva) (acceptedVersion, other-oa)
- Pure Amsterdam UMC (submittedVersion, other-oa)
- Radboud Repository (Radboud University) (submittedVersion)
- HAL (submittedVersion, other-oa)
- UCL Discovery (University College London) (submittedVersion)
- Università Politecnica delle Marche (Università Politecnica delle Marche) (submittedVersion)
- Lund University Publications (Lund University) (submittedVersion)
- VU Research Portal (submittedVersion, other-oa)
- Archive ouverte UNIGE (University of Geneva) (submittedVersion, cc-by)
- Research Publications (Maastricht University) (submittedVersion, other-oa)
- Data Archiving and Networked Services (DANS) (submittedVersion, other-oa)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Funders
- Interreg (SFC, 2016-202)
- National Institutes of Health (P01AG043362, U01 AG024904)
- Seventh Framework Programme (FP7/2007-2013)
- U.S. Department of Defense (W81XWH-12-2-0012)
- Vetenskapsrådet (2015-02830, 2013-8717)
- Forskningsrådet om Hälsa, Arbetsliv och Välfärd (2013-2496, 2013-2300, 2010-0870, 2012-1138)
- Sahlgrenska Universitetssjukhuset (ALF 716681)
- Alzheimer's Association (ZEN-01-3151, IIRG-00-2159)
- European Commission (QLK6-CT-2002-02645)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Clinical Neurology › Amyotrophic Lateral Sclerosis Research
- Keywords
- Alzheimer's disease, disease duration
- MeSH terms
- Aged, Alleles, Alzheimer Disease, Amyloid, Female, Genotype, Humans, Longitudinal Studies, Male, Sex Factors, Time Factors, Biomarkers, tau Proteins, Disease Progression, Positron-Emission Tomography, Apolipoprotein E4, Cognitive Dysfunction, Prodromal Symptoms
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-10-06, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-06 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Cited sources are checked with a language model’s help (gpt-6-sol).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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