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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.
Checked 2026-10-06 · 1 reference not checked yet
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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
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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
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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
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“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
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“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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“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).
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“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
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“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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“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
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“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
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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
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“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
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“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
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“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
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“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
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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
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“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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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
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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
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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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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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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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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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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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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
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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
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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.
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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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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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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.
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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.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
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.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — 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.
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.
- Checkable: passes — It can be checked against evidence.
- 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
“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.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — 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.
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.
- Checkable: passes — It can be checked against evidence.
- 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.
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.
- Checkable: passes — It can be checked against evidence.
- 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.
None of the sources cited for this claim have been checked yet.
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
- 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 [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 source
- Not checked yetcites [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 source
- 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 [12] Vos SJ,, Preclinical Alzheimer's disease and its outcome: a longitudinal cohort study. Lancet Neurol, 2013 12(10): p. 957– 65. 24012374 PMC3904678 source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: fails — It may be too vague to check against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may be too vague to check against evidence. It may state two separate claims as one.
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.
- Checkable: passes — It can be checked against evidence.
- 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
“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.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — 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.
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.
- Checkable: passes — It can be checked against evidence.
- 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
“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.
- Checkable: passes — It can be checked against evidence.
- 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.
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.
- Checkable: passes — It can be checked against evidence.
- 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.
- Checkable: passes — It can be checked against evidence.
- 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.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
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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Self-citationNIA‐AA Research Framework: Toward a biological definition of Alzheimer's disease
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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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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
Sorted by citations
Items 201–300 of 575
Wiest, I., Wiemers, T., Kraus, M.-J., Neeb, H., Strasser, E. F., Hausner, L., Frölich, L., & Bugert, P. (2019) · Journal of Alzheimer s Disease · doi:10.3233/jad-190574 · Cited by 16
“Among this population, roughly 10% might be diagnosed with preclinical AD, if investigated for brain amyloid load (calculated from incidence of AD and duration of preclinical AD) [42, 43].”
Zhang, Z., Wang, T., Hu, Z., Yang, L.-Z., & Li, H. (2025) · IEEE Journal of Biomedical and Health Informatics · doi:10.1109/jbhi.2024.3509620 · Cited by 17
“On the other hand, the damage caused by AD is progressive and irreversible, with no effective treatment currently available [4], [5].”
Wang, T., Arnold, M., Huynh, K., Weinisch, P., Giles, C., Mellett, N. A., Duong, T., Marella, B., Nho, K. T., Livera, A. M. D., et al. (2025) · EBioMedicine · doi:10.1016/j.ebiom.2025.105826 · Cited by 19
Observational studies in Alzheimer disease: bridging preclinical studies and clinical trials
Brenowitz, W. D., & Yaffe, K. S. (2022) · Nature Reviews Neurology · doi:10.1038/s41582-022-00733-7 · Cited by 16
Patterns of use of symptomatic treatments for Alzheimer's disease dementia (AD)
DiBello, J. R., Lü, Y., Swartz, J., Bortnichak, E. A., Liaw, K., Zhong, W., & Liu, X. (2023) · BMC Neurology · doi:10.1186/s12883-023-03447-5 · Cited by 15
“Based on the degree of cognitive impairment, AD is often divided into three stages: the preclinical stage, characterized by normal cognitive ability, the prodromal stage, characterized by mild cognitive impairment (MCI), and the dementia stage, with functional impairment [3].”
BackgroundBakhtiari, A., Benedek, K., Law, I. G., Fagerlund, B., Mortensen, E. L., Osler, M., Lauritzen, M., Larsson, H. B. W., & Vestergaard, M. B. (2023) · GeroScience · doi:10.1007/s11357-023-01031-w · Cited by 17
Hartz, S. M., Schindler, S., Streitz, M. L., Moulder, K., Mozersky, J. T., Wang, G.-Q., Xiong, C.-J., & Morris, J. (2025) · Alzheimer's & Dementia · doi:10.1002/trc2.70033 · Cited by 21
Application of artificial intelligence in Alzheimer’s disease: a bibliometric analysis
Song, S., Li, T., Lin, W., Liu, R., & Zhang, Y. (2025) · Frontiers in Neuroscience · doi:10.3389/fnins.2025.1511350 · Cited by 17
The Role of Dementia Diagnostic Delay in the Inverse Cancer–Dementia Association
Hayes‐Larson, E., Shaw, C. L., Ackley, S. F., Zimmerman, S. C., Glymour, M. M., Graff, R. E., Witte, J. S., Kobayashi, L. C., & Mayeda, E. R. (2021) · The Journals of Gerontology Series A · doi:10.1093/gerona/glab341 · Cited by 13
Olatunji, S. O., Alansari, A., Alkhorasani, H., Alsubaii, M., Sakloua, R., Alzahrani, R., Alsaleem, Y., Alassaf, R. A., Farooqui, M., Ahmed, M. I. B., et al. (2022) · Computational Intelligence and Neuroscience · doi:10.1155/2022/5476714 · Cited by 15
Gregory, S., Saunders, S., & Ritchie, C. W. (2022) · The Lancet Healthy Longevity · doi:10.1016/s2666-7568(22)00219-7 · Cited by 16
Deep learning based neuronal soma detection and counting for Alzheimer's disease analysis
Li, Q., Zhang, Y., Liang, H., Gong, H., Jiang, L., Liu, Q., & Shen, L. (2021) · Computer Methods and Programs in Biomedicine · doi:10.1016/j.cmpb.2021.106023 · Cited by 15
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“AD manifests insidiously and poses early diagnostic challenges, leading to cognitive deficits, psychiatric and behavioral problems, and the deterioration of social and daily life functions, ultimately resulting in death, typically occurring within 5 – 12 years of onset (Vermunt et al., 2019).”
Update on Major Neurocognitive Disorders
Jones, K. C. (2021) · FOCUS The Journal of Lifelong Learning in Psychiatry · doi:10.1176/appi.focus.20210004 · Cited by 17
Impact of Pneumonia on Cognitive Aging: A Longitudinal Propensity-Matched Cohort Study
Hendel, M. K., Rizzuto, D., Grande, G., Calderón‐Larrañaga, A., Laukka, E. J., Fratiglioni, L., & Vetrano, D. L. (2022) · The Journals of Gerontology Series A · doi:10.1093/gerona/glac253 · Cited by 15
“After 70, the risk of developing dementia increases significantly (7).”
BackgroundTargeting the molecular web of Alzheimer’s disease: unveiling pathways for effective pharmacotherapy
Jadhav, D., Saraswat, N., Vyawahare, N. S., & Shirode, D. S. (2024) · The Egyptian Journal of Neurology Psychiatry and Neurosurgery · doi:10.1186/s41983-023-00775-8 · Cited by 17
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“[9].”
Andújar, B. T., Mary, A., Venegas, C., Cheng, T., Zaslavsky, L. Y., Bolton, E., Heneka, M. T., & Schymanski, E. (2024) · Environmental Science & Technology · doi:10.1021/acs.est.3c10490 · Cited by 13
Wen, Q., Wittens, M. M. J., Engelborghs, S., van Herwijnen, M. H. M., Tsamou, M., Roggen, E., Smeets, H. J. M., Krauskopf, J., & Briedé, J. J. (2024) · ACS Chemical Neuroscience · doi:10.1021/acschemneuro.3c00740 · Cited by 14
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RNA‐Based Therapies for Neurodegenerative Diseases Targeting Pathogenic Proteins
Rabbani, S. A., El‐Tanani, M., Sharma, S., El‐Tanani, Y., Kumar, R., Saini, M., Yadav, M., Khan, M. A., & Parvez, S. (2025) · European Journal of Neuroscience · doi:10.1111/ejn.70110 · Cited by 15
“These brain pathologies can be quantified in vivo using specific biomarkers for Aβ and τ (Jack et al. 2018), and this stage may persist for 20 to 30 years without clinical symptoms (Vermunt et al. 2019).”
Fighting fire with fire: The immune system might be key in our fight against Alzheimer’s disease
Dujardin, P., Vandenbroucke, R. E., & Hoecke, L. V. (2022) · Drug Discovery Today · doi:10.1016/j.drudis.2022.01.004 · Cited by 14
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“As the disease progresses, patients first develop memory impairment and gradually progress to MCI (stage 3) [45], with involvement of the hippocampus, insula, amygdala, and other brain regions [46–51].”
Motoric cognitive risk syndrome trajectories and incident dementia over 10 years
Mullin, D. S., Gadd, D. A., Russ, T. C., Michelle Luciano, A., & Terrera, G. M. (2023) · Cerebral Circulation - Cognition and Behavior · doi:10.1016/j.cccb.2023.100178 · Cited by 13
“It is vital to focus on identifying the early predementia stage as this is when addressing modifiable risk factors and organizing future care may be most effective at reducing the impact of dementia [1].”
BackgroundZou, Y., Gao, B., Lu, J., Zhang, K., Zhai, M., Yuan, Z., Aschner, M., Chen, J., Luo, W., Wang, L., et al. (2024) · Exploration · doi:10.1002/exp.20230154 · Cited by 13
Microglia in Neurodegenerative Diseases
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Understanding the Molecular Impact of Physical Exercise on Alzheimer’s Disease
Cantón-Suárez, A., Sánchez-Valdeón, L., Bello-Corral, L., Cuevas, M. J., & Estébanez, B. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms252413576 · Cited by 16
“…on the author, but essentially, in almost every staging system, the disease starts with preclinical AD as an asymptomatic phase with biomarker signs of AD, progresses to mild cognitive impairment (MCI) and/or mild behavioural impairment (MBI), and eventually concludes with AD dementia [27–29].”
Lin, C.-Y., Zhai, Y.-J., An, H.-H., Wu, F., Qiu, H.-N., Li, J.-B., & Lin, J. (2025) · Scientific Reports · doi:10.1038/s41598-025-97404-6 · Cited by 14
“In fact, the preclinical stage of AD already shows abnormal accumulation of amyloid-β and hyper-phosphorylated tau proteins 37 .”
Matziorinis, A. M., Flo, B. K., Skouras, S., Dahle, K., Henriksen, A., Hausmann, F., Sudmann, T. T., Gold, C., & Koelsch, S. (2023) · Pilot and Feasibility Studies · doi:10.1186/s40814-023-01287-1 · Cited by 19
Translating Alzheimer’s Disease Mechanisms into Therapeutic Opportunities
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“According to a multicenter study, the duration of AD is about 20 years in total, including mild cognitive impairment (MCI), the preclinical stage, and the dementia stage [1].”
Salcedo‐Arellano, M. J., Sanchez, D., Wang, J. Y., McLennan, Y. A., Clark, C. J., Juárez, P., Schneider, A., Tassone, F., Hagerman, R. J., & Martínez‐Cerdeño, V. (2021) · Frontiers in Neuroscience · doi:10.3389/fnins.2021.720253 · Cited by 13
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Diagnosis of Alzheimer's disease: Towards accuracy and accessibility
Mu, Y., Chang, K., Chen, Y.-F., Yan, K., Wang, C.-X., & Hua, Q. (1970) · Journal of Biological Methods · doi:10.14440/jbm.2024.412 · Cited by 13
“Therefore, Aβ plaques are considered to be the main pathological marker of AD [28-30].”
BackgroundНаволокин, Н. А., Adushkina, V., Zlatogorskaya, D., Telnova, V., Evsukova, A., Vodovozova, E. L., Anna, E., Dosadina, E. E., Diduk, S., & Semyachkina-Glushkovskaya, O. V. (2024) · Pharmaceuticals · doi:10.3390/ph17060788 · Cited by 13
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Recent advances in pre-clinical diagnosis of Alzheimer’s disease
Zhou, J., Benoit, M., & Sharoar, M. G. (2021) · Metabolic Brain Disease · doi:10.1007/s11011-021-00733-4 · Cited by 14
“Behavioral and cognitive dysfunction dramatically increase in late life leading to an inevitable death outcome within 5– 12 years of symptomatic appearance (McKhann et al. 2011; Vermunt et al. 2019).”
BackgroundGanguly, D., Thomas, J. A., Ali, A., & Kumar, R. K. (2022) · European Journal of Neuroscience · doi:10.1111/ejn.15591 · Cited by 12
Accelerated midlife endocrine and bioenergetic brain aging in APOE4 females
Wang, T., Mao, Z., Shang, Y., Merlini, S., Vitali, F., Wiegand, J. L., & Brinton, R. D. (2025) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2025.1632877 · Cited by 12
Demirbilek, O., & Rekik, I. (2022) · Medical Image Analysis · doi:10.1016/j.media.2022.102649 · Cited by 11
“Additionally, several neurological disorders, such as AD, may have multiple early stages (e.g., mild cognitive impairment), each observed at a particular timepoint (Braak and Braak, 1991; Wesseling et al., 2020; Vermunt et al., 2019).”
Daou, L., Alayli, A. E., Constantinos, F., Dib, G., & Barakat, M. (2023) · Biomarkers in Neuropsychiatry · doi:10.1016/j.bionps.2023.100069 · Cited by 11
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“Moreover, it is important to note that the duration of each stage in AD was influenced by age, sex, and APOE genotype (Vermunt et al., 2019).”
BackgroundReid, G., Vassilev, P., Irving, J., Ojakäär, T., Jacobson, L., Lawrence, E. G., Barnett, J., Tapparel, M., & Koychev, I. G. (2024) · The British Journal of Psychiatry · doi:10.1192/bjp.2024.18 · Cited by 11
“A fuller summary of responses to the eight Likert-style questions can be found in Supplementary material 6.”
BackgroundSystemic inflammation, lifestyle behaviours and dementia: A 10-year follow-up investigation
Hillari, L., Frank, P., & Cadar, D. (2024) · Brain Behavior & Immunity - Health · doi:10.1016/j.bbih.2024.100776 · Cited by 10
Somatostatin: Linking Cognition and Alzheimer Disease to Therapeutic Targeting
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Wang, Y., Li, M., Haughton, D., & Kazis, L. E. (2024) · PLoS ONE · doi:10.1371/journal.pone.0306270 · Cited by 12
“In recent years, this approach has been introduced to study the progression of AD [27–31].”
MethodBiological mechanisms of resilience to tau pathology in Alzheimer’s disease
Svenningsson, A. L., Bocancea, D. I., Stomrud, E., van Loenhoud, A. C., Barkhof, F., Mattsson, N., Palmqvist, S., Hansson, O., & Ossenkoppele, R. (2024) · Alzheimer s Research & Therapy · doi:10.1186/s13195-024-01591-9 · Cited by 12
“…between time and tau PET were included in all analyses, covarying for age, sex, and mean NPX, as well as their interactions with time (as the longitudinal accumulation of tau pathology and time to disease progression can differ between males and females or participants of different ages [55, 56]).”
Rigotto, G., Zentilin, L., Pozzan, T., & Basso, E. (2021) · Cells · doi:10.3390/cells10082046 · Cited by 12
“Clinical symptoms are cognitive impairment and dementia characterized by progressive, profound disability culminating with death [2–4]; it is proposed that subtle alterations in the physiology of the brain and the so-called preclinical phase might precede the overt manifestation of clinical symptoms by 2–3 decades [5].”
BackgroundLee, S.-S., McGrattan, A., Soh, Y. C., Alawad, M., Su, T. T., Palanisamy, U., Hussin, A. M., Kassim, Z. B., Ghazali, A. N. B. M., Stephan, B. C. M., et al. (2022) · Nutrients · doi:10.3390/nu14030430 · Cited by 12
Hypertension and cognitive function: a review of life-course factors and disparities
Anda‐Duran, I. D., Woltz, S. G., Bell, C. N., & Bazzano, L. (2022) · Current Opinion in Cardiology · doi:10.1097/hco.0000000000000975 · Cited by 13
Amylin and Secretases in the Pathology and Treatment of Alzheimer’s Disease
Singh, S. P., Yang, F., Sivils, A., Cegielski, V., & Chu, X. (2022) · Biomolecules · doi:10.3390/biom12070996 · Cited by 11
“Clinically, it presents in three stages of cognition sequencing from normal ability to functional impairment and memory loss, colloquially known as dementia [3].”
BackgroundMank, A., van Maurik, I. S., Rijnhart, J. J. M., Bakker, E. D., Bouteloup, V., Scouarnec, L. L., Teunissen, C. E., Barkhof, F., Scheltens, P., Berkhof, J. H., et al. (2022) · Alzheimer s Research & Therapy · doi:10.1186/s13195-022-01053-0 · Cited by 11
“The largest part of the AD disease process takes place before the stage of dementia, but studies on prognosis in terms of institutionalization and mortality in pre-dementia stages are hardly available [14].”
BackgroundSelf-citationPredicting sojourn times across dementia disease stages, institutionalization, and mortality
Tate, A., Bouteloup, V., van Maurik, I. S., Jean, D., Mank, A., Špeh, A., Boilet, V., van Harten, A. C., Eriksdotter, M., Wimo, A. B., et al. (2023) · Alzheimer s & Dementia · doi:10.1002/alz.13488 · Cited by 11
“11 However, with just over 3000 participants, they were unable to fully examine the later stages of AD and mortality.”
BackgroundContributions of Molecular and Optical Techniques to the Clinical Diagnosis of Alzheimer’s Disease
Bistaffa, E., Tagliavini, F., Matteini, P., & Moda, F. (2020) · Brain Sciences · doi:10.3390/brainsci10110815 · Cited by 11
“with progressive impairment of physiological functions, and the death generally occurs within 5–12 years from symptoms onset [10].”
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Amyloid-β-driven Alzheimer’s disease reshapes the colonic immune system in mice
Makhijani, P., Valentino, T. R., Manwaring-Mueller, M., Emani, R., Mu, W., Aguirre, C. G., Tan, C. R., Rane, A., Wilson, K. A., Kifle, A., et al. (2025) · Cell Reports · doi:10.1016/j.celrep.2025.116109 · Cited by 13
“13 This stage has been the subject of intense study to better understand the underlying risk factors, identify early diagnosis biomarkers, and implement preventative interventions.”
Chen, B.-A., Lee, W., Chung, C., Peng, L., & Chen, L. (2022) · The Journal of Prevention of Alzheimer s Disease · doi:10.14283/jpad.2022.83 · Cited by 10
“Clinically, the ApoE e4 allele was associated with small vessel disease and atherosclerosis, and ApoE e4 allele carriers experienced faster cognitive declines in the preclinical stage (23, 25).”
BackgroundMethodRudnitskaya, E. A., Kozlova, T., Burnyasheva, A. O., Peunov, D., Tyumentsev, M., Stefanova, N. A., & Kolosova, N. G. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms242115649 · Cited by 10
“Recent studies involving state-of-the-art diagnostic techniques have confirmed that the preclinical period of the sporadic type (>95% of cases [2]) of AD can last for decades [3], but the question of when exactly disease development begins and what contributes to it remains open.”
BackgroundChen, Y., Li, W., & Yang, H. (2024) · Frontiers in Public Health · doi:10.3389/fpubh.2023.1338665 · Cited by 10
Kress, G. T., Popa, E. S., Merrill, D. A., Bramen, J. E., & Siddarth, P. (2024) · Neuroreport · doi:10.1097/wnr.0000000000002037 · Cited by 10
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Liang, Z., Qin, H., Su, B., Bao, Y., Vitiello, M. V., Hu, G., & Wang, Y. (2025) · Obesity · doi:10.1002/oby.24208 · Cited by 9
“First, the conflicting findings may be attributable to reverse causation due to weight loss during the preclinical and prodromal phase of dementia [7], thus leading to biased association.”
Hypothalamic volume, sleep, and APOE genotype in cognitively healthy adults
Laurell, A. A. S., Mak, E., Dounavi, M., Underwood, B. R., Dauvilliers, Y. A., Dudas, R. B., Marguet, O. E., Ritchie, C. W., Koychev, I. G., LAWLOR, B. A., et al. (2025) · Alzheimer s & Dementia · doi:10.1002/alz.70244 · Cited by 10
“68 Wealsoobservedasignificanteffectofsexonhypothalamicvolume, with men having significantly larger hypothalamic volume compared to women, but also show a greater age-associated volume loss for almost all subunits.”
Palmer, J. A., Kaufman, C. S., Vidoni, E. D., Honea, R. A., Burns, J. M., & Billinger, S. A. (2022) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2022.02.014 · Cited by 11
Sensory impairment and algorithmic classification of early cognitive impairment
Cai, Y., Schrack, J. A., Gross, A. L., Armstrong, N. M., Swenor, B. K., Deal, J. A., Lin, F. R., Wang, H., Tian, Q., An, Y., et al. (2023) · Alzheimer s & Dementia Diagnosis Assessment & Disease Monitoring · doi:10.1002/dad2.12400 · Cited by 9
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Predicting age at Alzheimer's dementia onset with the cognitive clock
Yu, L., Wang, T., Wilson, R. S., Guo, W., Aggarwal, N. T., Bennett, D. A., & Boyle, P. A. (2023) · Alzheimer s & Dementia · doi:10.1002/alz.13004 · Cited by 11
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Cannon, E. J., Windham, B. G., Griswold, M. E., Palta, P., Knopman, D. S., Sedaghat, S., & Lutsey, P. L. (2025) · Neurology · doi:10.1212/wnl.0000000000213534 · Cited by 9
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Stuebs, J., Langballe, E. M., Livingston, G., Anstey, K. J., Deckers, K., Mathews, F. E., Mika Kivimaki, B., Strand, B. H., Rokstad, A. M. M., Krokstad, S., et al. (2025) · The Journal of Prevention of Alzheimer s Disease · doi:10.1016/j.tjpad.2025.100326 · Cited by 9
“…or longer than in most previous validation studies [21], providing a more comprehensive assessment of long-term dementia risk prediction and reduced likelihood of reverse causality, as the follow-up period exceeds the average duration of the pre-clinical stage of dementia measured at age 70 [51].”
Mullin, D. S., Stirland, L., Russ, T. C., Michelle Luciano, A., & Terrera, G. M. (2023) · European Journal of Neurology · doi:10.1111/ene.15731 · Cited by 9
“Much research now focuses on identifying the early predementia stages when intervention may be most effective [1].”
Sleep behavior traits and associations with opioid-related adverse events: a cohort study
Chen, R. W., Ulsa, M. C., Li, P., Gao, C., Zheng, X., Xu, J., Luo, Y., Shen, S., Lane, J. M., Scheer, F. A. J. L., et al. (2023) · SLEEP · doi:10.1093/sleep/zsad118 · Cited by 11
Categorical predictive and disease progression modeling in the early stage of Alzheimer’s disease
Platero, C. A. (2022) · Journal of Neuroscience Methods · doi:10.1016/j.jneumeth.2022.109581 · Cited by 8
“The risk of progression from CU to MCI/dementia depends on a number of factors, including age, sex, and apolipoprotein E (APOE) status (Vermunt et al., 2019).”
BackgroundCalderón‐Garcidueñas, L. (2022) · Frontiers in Neurology · doi:10.3389/fneur.2022.901447 · Cited by 9
“We also have a significant controversy with the duration of preclinical, prodromal, and dementia stages (47), since we are detecting cognitive deficits in childhood associated with structural brain alterations and progressively worse cognition in young adults with abnormal brain MRIs (48).”
BackgroundZou, Y., Yu, S., Ma, X., Ma, C., Mao, C., Mu, D., Li, L., Gao, J., & Qiu, L. (2022) · Clinical Biochemistry · doi:10.1016/j.clinbiochem.2022.11.013 · Cited by 9
Amyloid toxicity in a Drosophila Alzheimer's model is ameliorated by autophagy activation
Tsakiri, E. N., Gumeni, S., Manola, M. S., & Trougakos, I. P. (2021) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2021.04.017 · Cited by 9
Iron Responsive Element (IRE)-mediated responses to iron dyshomeostasis in Alzheimer’s diseasePreprint
Hin, N., Newman, M., Pederson, S., & Lardelli, M. T. (2020) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2020.05.01.071498 · Cited by 9
Wu, L., Arvai, S., Wang, S. J., Liu, A., & Xu, B. (2024) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2023.1288930 · Cited by 9
Biofluid biomarkers for Alzheimer’s disease
Wang, S., Xie, S., Zheng, Q., Zhang, Z., Wang, T., & Zhang, G. (2024) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2024.1380237 · Cited by 9
Akkaya, D., Seyhan, G., Sarı, S., & Barut, B. (2024) · Drug Development Research · doi:10.1002/ddr.22184 · Cited by 8
“The insidious nature of AD unfolds through distinct stages, encompassing the early phase, the middle stage, and finally culminating in the late dementia phase, with an estimated total duration extending over two decades (Long et al., 2024; Vermunt et al., 2019).”
BackgroundBrijnath, B., Markusevska, S., Lock, K., Doherty, K., Eccleston, C. E. A., Navarro, C., Gilbert, A. S., Antoniades, J., & Cavuoto, M. G. (2025) · Clinical Gerontologist · doi:10.1080/07317115.2025.2453710 · Cited by 8
“As the gradual progression of brain pathology is ~15–25 years before dementia onset (Vermunt et al., 2019), efforts to reduce dementia risk must target the entire life-course and therefore, a whole of population approach is needed.”
Monitoring Acidification Preceding Aβ Deposition in Alzheimer's Disease
Zhu, G., Zhang, H., Xie, R., Younis, M. R., Fu, S., Wang, X., Liu, B., Li, K., Lui, S., & Wu, M. C. (2025) · Advanced Healthcare Materials · doi:10.1002/adhm.202404907 · Cited by 8
Healthcare Complexities in Neurodegenerative Proteinopathies: A Narrative Review
Fereshtehnejad, S., & Lökk, J. (2025) · Healthcare · doi:10.3390/healthcare13151873 · Cited by 11
“In AD, the prodromal phase can span decades, characterized by early accumulation of amyloid-beta and tau pathology in the brain [44].”
Pathological Mechanisms and Molecular Imaging Advances in Alzheimer’s Disease
Liu, C., Meng, Y., Liu, R., Wang, Z., & Zhao, H. (2025) · Clinical Interventions in Aging · doi:10.2147/cia.s534015 · Cited by 8
“55 Therefore, PET imaging is currently employed for the early clinical diagnosis of AD.”
The clinical characteristics and subtypes of patients with cognitive impairment in memory clinic
Liu, S., Gan, J., Hu, W., Wang, X., Zhu, H., Du, X., Shi, Z., Huang, G., & Ji, Y. (2020) · Journal of Clinical Neuroscience · doi:10.1016/j.jocn.2020.10.031 · Cited by 8
O espectro clínico e laboratorial da doença de Alzheimer
Moreira, M. A., & Moreira, S. V. (2020) · Revista Psicologia em Pesquisa · doi:10.34019/1982-1247.2020.v14.30649 · Cited by 11
Cognitive Writing Process Characteristics in Alzheimer’s Disease
Meulemans, C., Leijten, M., Waes, L. V., Engelborghs, S., & Mæyer, S. D. (2022) · Frontiers in Psychology · doi:10.3389/fpsyg.2022.872280 · Cited by 10
A Transgenic 5xFAD-M Line of Mice for Dendritic Spine Morphology Analysis in Alzheimer’s Disease
Ilina, A., & Linkova, N. S. (2023) · Brain Sciences · doi:10.3390/brainsci13020307 · Cited by 9
“AD is associated with the progressive disability of patients, causing death 5–12 years after symptom onset [6].”
BackgroundZagorski, K., King, O., Hovakimyan, A., Petrushina, I., Antonyan, T., Chailyan, G., Ghazaryan, M., Hyrc, K. L., Chadarevian, J. P., Davtyan, H., et al. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24129797 · Cited by 8
Antagonistic Roles of P2X7 and P2Y2 Receptors in Neurodegenerative Diseases
Glaser, T., Oliveira‐Giacomelli, Á., Petiz, L. L., Ribeiro, D. E., Andrejew, R., & Ulrich, H. (2021) · Frontiers in Pharmacology · doi:10.3389/fphar.2021.659097 · Cited by 8
“Aβ aggregation triggers neuroinflammation in AD, as patients may have Aβ deposits as early as 10 years prior to first AD symptoms (Vermunt et al., 2019).”
BackgroundLooking at Alzheimer’s Disease Pathogenesis from the Nuclear Side
D’Andrea, L., Stringhi, R., Luca, M. D., & Marcello, E. E. (2021) · Biomolecules · doi:10.3390/biom11091261 · Cited by 8
A New Insight on Feasibility of Pre-, Pro-, and Synbiotics-based Therapies in Alzheimer’s Disease
Talebi, M., Ebrahimi, V., Rasouli, A., Farjami, A., Soofiyani, S. R., Soleimanian, A., Forouhandeh, H., & Tarhriz, V. (2022) · Journal of Reports in Pharmaceutical Sciences · doi:10.4103/jrptps.jrptps_170_21 · Cited by 8
Diagnostic groups of hospital stays and outpatient visits during 10 years before Alzheimer’s disease
Mäklin, K., Lampela, P., Lin, J., Sirpa, H., & Tolppanen, A. (2023) · BMC Health Services Research · doi:10.1186/s12913-023-09345-3 · Cited by 8
Munoz, S. R., de Vries, S. T., Lankester, G., Pignatti, F., Munster, B. C. V., Radford, I., Guizzaro, L., Mol, P. G. M., Hillege, H. L., & Postmus, D. (2023) · The Journal of Prevention of Alzheimer s Disease · doi:10.14283/jpad.2023.84 · Cited by 7
“The levels of the attributes were based on previous literature (7, 8, 32) and the input of people living with MCI.”
MethodAye, S., Frisell, O., Zetterberg, H., Skillbäck, T. B., Kern, S., Eriksdotter, M., Aho, E., Xia, X., Winblad, B. G., Wimo, A. B., et al. (2024) · PharmacoEconomics · doi:10.1007/s40273-024-01443-2 · Cited by 9
Self-citationDocumentation of prodromal features and risk factors of dementia disease in primary care practice
Michalowsky, B., Teipel, S. J., Riedel-Heller, S. G., Kostev, K., & Bohlken, J. (2024) · Journal of Alzheimer s Disease · doi:10.1177/13872877241295407 · Cited by 7
“4,15,16 This study demonstrated that primary care physicians documented these features fi ve to ten years beforetheincidentdementiadiagnosis.”
Non-Drug and Non-Invasive Therapeutic Options in Alzheimer’s Disease
Şovrea, A. S., Boşca, A. B., Dronca, E., Constantin, A.-M., Crintea, A., Suflețel, R. T., Lupean, R.-A., Ștefan, P.-A., Onofrei, M. M., Tschall, C., et al. (2025) · Biomedicines · doi:10.3390/biomedicines13010084 · Cited by 9
“AD dementia is manifested by significant and progressive disabilities throughout the disease, with death occurring within 5–12 years of the onset of symptoms [7].”
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).
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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