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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
Jack, C. R., Bennett, D. A., Blennow, K., Carrillo, M. C., Dunn, B., Haeberlein, S. B., Holtzman, D. M., Jagust, W., Jessen, F., Karlawish, J., et al. (2018) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2018.02.018 · Cited by 10,537
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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
Sperling, R. A., Aisen, P. S., Beckett, L. A., Bennett, D. A., Craft, S., Fagan, A. M., Iwatsubo, T., Jack, C. R., Kaye, J., Montine, T. J., et al. (2011) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2011.03.003 · Cited by 7,155
Winblad, B., Palmer, K., Kivipelto, M., Jelic, V., Fratiglioni, L., Wahlund, L. ‐., Nordberg, A., Bäckman, L., Albert, M., Almkvist, O., et al. (2004) · Journal of Internal Medicine · doi:10.1111/j.1365-2796.2004.01380.x · Cited by 4,946 · cited 1×
“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
Sorted by citations
Items 101–200 of 575
Ha, J., Choi, D., Kim, K. J., Kim, K. Y., Nam, C. M., & Kim, E. (2023) · Neurology · doi:10.1212/wnl.0000000000207069 · Cited by 36
Newby, D., Linden, A. B., Fernandes, M., Winchester, L. M., Molero, Y., Sproviero, W., Ghose, U., Li, Q. S., Launer, L. J., van Duijn, C. M., et al. (2022) · BMJ Open Diabetes Research & Care · doi:10.1136/bmjdrc-2022-003036 · Cited by 35
Rizzo, S. J. S., Homanics, G. E., Schaeffer, D. J., Schaeffer, L. K. H., Park, J. E., Oluoch, J., Zhang, T., Haber, A., Seyfried, N. T., Paten, B., et al. (2023) · Alzheimer s & Dementia Translational Research & Clinical Interventions · doi:10.1002/trc2.12417 · Cited by 40
Posterity of nanoscience as lipid nanosystems for Alzheimer's disease regression
Naser, S. S., Singh, D., Preetam, S., Kishore, S., Kumar, L., Nandi, A., Simnani, F. Z., Choudhury, A., Sinha, A., Mishra, Y. K., et al. (2023) · Materials Today Bio · doi:10.1016/j.mtbio.2023.100701 · Cited by 37
Gessi, S., Poloni, T. E., Negro, G., Varani, K., Pasquini, S., Vincenzi, F., Borea, P. A., & Merighi, S. (2021) · Cells · doi:10.3390/cells10092344 · Cited by 36
Kulichikhin, K. Y., Fedotov, S. A., Rubel, M. S., Zalutskaya, N. M., Zobnina, A. E., Malikova, O. A., Незнанов, Н. Г., Chernoff, Y. O., & Rubel, A. A. (2021) · Prion · doi:10.1080/19336896.2021.1917289 · Cited by 34
Disease- and stage-specific alterations of the oral and fecal microbiota in Alzheimer's disease
Troci, A., Philippen, S., Rausch, P., Rave, J., Weyland, G., Niemann, K., Jessen, K., Schmill, L.-P. A., Aludin, S., Franke, A., et al. (2023) · PNAS Nexus · doi:10.1093/pnasnexus/pgad427 · Cited by 33
“In AD, neurodegenerative processes start decades before clinical symptoms emerge (Jack et al., 2010; Vermunt et al., 2019) resulting in a preclinical stage of AD.”
BackgroundEstimating demand for potential disease-modifying therapies for Alzheimer's disease in the UK
Laurell, A. A. S., Venkataraman, A. V., Schmidt, T., Montagnese, M., Mueller, C., Stewart, R. J., Lewis, J. R., Mundell, C., Isaacs, J. D., Krishnan, M. S., et al. (2024) · The British Journal of Psychiatry · doi:10.1192/bjp.2023.166 · Cited by 32
“Although the additional exclusion criteria might reduce the potential treatment population further, we do not have data to address all of them and it seems unlikely any one would exclude a large number of patients, so we did not adjust the total potential treatment population.”
BackgroundSchilling, L. P., Balthazar, M. L. F., Radanovic, M., Forlenza, O. V., Silagi, M. L., Smid, J., Barbosa, B. J. A. P., Frota, N. A. F., de Souza, L. C., Vale, F. A. C., et al. (2022) · Dementia & Neuropsychologia · doi:10.1590/1980-5764-dn-2022-s102pt · Cited by 59
Malzbender, K., Barbarino, P., Ferrell, P. B., Bradshaw, A. C., Brookes, A. J., Díaz, C., van der Flier, W. M., Georges, J., Hansson, O., Hartmanis, M. G. N., et al. (2024) · The Journal of Prevention of Alzheimer s Disease · doi:10.14283/jpad.2024.32 · Cited by 29
“Given the slow, gradual progression of AD neuropathology from an asymptomatic stage or before symptoms are detectable with cognitive tests (preclinical AD) to mild cognitive impairment (prodromal AD) to dementia (the end-stage of AD) there is a window of opportunity for early intervention (15).”
BackgroundSelf-citationHayes‐Larson, E., Ackley, S. F., Zimmerman, S. C., Ospina‐Romero, M., Glymour, M. M., Graff, R. E., Witte, J. S., Kobayashi, L. C., & Mayeda, E. R. (2020) · Alzheimer s & Dementia · doi:10.1002/alz.12168 · Cited by 29
The Protective A673T Mutation of Amyloid Precursor Protein (APP) in Alzheimer’s Disease
Xia, Q., Yang, X., Shi, J., Liu, Z., Peng, Y., Wang, W., Li, B., Zhao, Y., Xiao, J., Huang, L. F., et al. (2021) · Molecular Neurobiology · doi:10.1007/s12035-021-02385-y · Cited by 32
Zarhin, D., Atsmon, R., Ruggiero, A., Baeloha, H., Shoob, S., Scharf, O., Heim, L. R., Buchbinder, N., Shinikamin, O., Shapira, I., et al. (2022) · Cell Reports · doi:10.1016/j.celrep.2021.110268 · Cited by 32
“However, the onset of amyloid-b (Ab) depositions precedes cognitive impairments by at least 10– 20 years, marking a significant presymptomatic disease stage (Bateman et al., 2012; Long and Holtzman, 2019; Vermunt et al., 2019).”
Backgroundvan der Veere, P. J., Hoogland, J., Visser, L. N. C., van Harten, A. C., Rhodius‐Meester, H. F. M., Sikkes, S. A. M., Venkatraghavan, V., Barkhof, F., Teunissen, C. E., van de Giessen, E., et al. (2024) · Neurology · doi:10.1212/wnl.0000000000209605 · Cited by 33
Self-citationFiciarà, E., Boschi, S., Ansari, S. A., D’Agata, F., Abollino, O., Caroppo, P., Fede, G. D., Indaco, A., Rainero, I., & Guiot, C. (2021) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2021.607858 · Cited by 29
“The duration of the preclinical and prodromal phase of AD varies from 10 to 20 years before clinical symptoms emerge (Vermunt et al., 2019).”
BackgroundAlzheimer and Purinergic Signaling: Just a Matter of Inflammation?
Merighi, S., Poloni, T. E., Terrazzan, A., Moretti, E., Gessi, S., & Ferrari, D. (2021) · Cells · doi:10.3390/cells10051267 · Cited by 30
“They depend on both non-modifiable genetic factors (pathogenic mutations in PSN-1-2 and APP genes, APO-E4 allele, AD-related polymorphisms) [23,24], and modifiable factors related to the individual’s history.”
BackgroundLife expectancy with and without dementia in persons with mild cognitive impairment in the community
Mooldijk, S. S., Yaqub, A., Wolters, F. J., Licher, S., Koudstaal, P. J., Ikram, M. K., & Ikram, M. A. (2021) · Journal of the American Geriatrics Society · doi:10.1111/jgs.17520 · Cited by 28
“Another study among participants with evidence of amyloid accumulation drawn from both clinic-based and researchbased cohorts confirmed a less favorable prognosis for participants in a clinical setting.(2) However, even participants with MCI from research-based cohorts were expected to live more than half of their rem…”
ResultAlzheimer's disease amyloid-β pathology in the lens of the eye
Moncaster, J. A., Moir, R. D., Burton, M. A., Chadwick, O., Minaeva, O. V., Alvarez, V. E., Ericsson, M., Clark, J. I., McKee, A. C., Tanzi, R. E., et al. (2022) · Experimental Eye Research · doi:10.1016/j.exer.2022.108974 · Cited by 30
Dubbelman, M. A., Hendriksen, H. M. A., Harrison, J., Vijverberg, E. G. B., Prins, N. D., Kroeze, L. A., Ottenhoff, L., van Leeuwenstijn, M. S. S. A., Verberk, I. M. W., Teunissen, C. E., et al. (2023) · Neurology · doi:10.1212/wnl.0000000000207978 · Cited by 27
Self-citationIntegrative Single-Plaque Analysis Reveals Signature Aβ and Lipid Profiles in the Alzheimer’s Brain
Enzlein, T., Lashley, T., Sammour, D. A., Hopf, C., & Chávez‐Gutiérrez, L. (2024) · Analytical Chemistry · doi:10.1021/acs.analchem.3c05557 · Cited by 28
The Impact of Ageing on the CNS Immune Response in Alzheimer’s Disease
Chee, S. E. J., & Solito, E. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.738511 · Cited by 29
Tarawneh, H. Y., Jayakody, D. M. P., Sohrabi, H. R., Martins, R. N., & Mulders, W. H. A. M. (2022) · Journal of Alzheimer s Disease Reports · doi:10.3233/adr-220035 · Cited by 30
“sion of each of these stages is not the same in each individual and it has been proposed that factors such as age of onset, genetic risk factors, and gender play a significant role in the duration of each stage [37].”
BackgroundZhou, Y., Yao, X.-Y., Han, W., Wang, Y., Li, Z., & Li, Y. (2022) · International Journal of Geriatric Psychiatry · doi:10.1002/gps.5827 · Cited by 26
“Among them, MCI is the intermediate stage between the cognitive changes of normal aging and dementia.(2) Apathy and depression are highly prevalent in older people with MCI.”
BackgroundAge-, sex-, and pathology-related variability in brain structure and cognition
Bachmann, D., Buchmann, A., Studer, S. T., Saake, A., Rauen, K., Zuber, I., Gruber, E., Nitsch, R. M., Höck, C., Gietl, A. F., et al. (2023) · Translational Psychiatry · doi:10.1038/s41398-023-02572-6 · Cited by 32
“Importantly, both neuropathological changes can be identified decades before clinical symptoms occur [6, 7] and emerging evidence suggests that AD- and vascular-related pathologies can have detrimental effects on brain structure and cognition already at low pathology burden [8–11].”
BackgroundPharmacological Treatment of Alzheimer’s Disease: Insights from Drosophila melanogaster
Cheng, X., Song, C., Du, Y., Gaur, U., & Yang, M. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21134621 · Cited by 28
“, constitute the main pathological hallmarks of AD [11-15].”
BackgroundChallenges in demonstrating the value of disease-modifying therapies for Alzheimer’s disease
Gustavsson, A., Pemberton-Ross, P. J., Montero, M. G., Hashim, M., & Thompson, R. (2020) · Expert Review of Pharmacoeconomics & Outcomes Research · doi:10.1080/14737167.2020.1822738 · Cited by 27
George, K. M., Gilsanz, P., Peterson, R. L., Barnes, L. L., DeCarli, C. S., Mayeda, E. R., Mungas, D., & Whitmer, R. A. (2021) · The Journals of Gerontology Series A · doi:10.1093/gerona/glab143 · Cited by 30
Iron Responsive Element-Mediated Responses to Iron Dyshomeostasis in Alzheimer’s Disease
Hin, N., Newman, M., Pederson, S., & Lardelli, M. T. (2021) · Journal of Alzheimer s Disease · doi:10.3233/jad-210200 · Cited by 28
Song, H., Yang, J., & Yu, W. (2022) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2021.825729 · Cited by 27
“Numerous longitudinal studies have demonstrated that AD pathology develops decades preceding onset of clinical symptoms (Vermunt et al., 2019).”
BackgroundObesity during preclinical Alzheimer's disease development exacerbates brain metabolic decline
Anderson, T., Sharma, S. K., Kelberman, M. A., Ware, C. B., Guo, N., Qin, Z. S., Weinshenker, D., & Parent, M. B. (2023) · Journal of Neurochemistry · doi:10.1111/jnc.15900 · Cited by 26
“…deteriorate, brain metabolism declines, and NFT pathology spreads to the hippocampus and temporal neocortex; dementia sets in as NFTs form throughout the cortex causing neu - ronal death (Braak et al., 2011 ; Braak & Braak, 1991; van der Kant et al., 2020 ; Vermunt et al., 2019; Weinshenker, 2018).”
BackgroundChavoshinezhad, S., Beirami, E., Izadpanah, E., Feligioni, M., & Hassanzadeh, K. (2023) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2023.115656 · Cited by 28
Pang, M., Gabelle, A., Saha‐Chaudhuri, P., Huijbers, W., Gafson, A., Matthews, P. M., Tian, L., Rubino, I., Hughes, R., de Moor, C., et al. (2023) · Alzheimer s & Dementia · doi:10.1002/alz.13431 · Cited by 27
“…APOE 𝜀 4 allele carrier status did not come out as a variable of significant importance despite its association with an increased risk of dementia 23–25 while a sensitivity analysis further refiningourITRscoremodeltoevaluatetheeffectofhomo-versushet-erozygousAPOE 𝜀…”
BackgroundUdeh‐Momoh, C. T., Maina, R., Anazodo, U., Akinyemi, R., Atwoli, L., Baker, L. D., Bassil, D. T., Blackmon, K., Bosire, E. N., Chemutai, G., et al. (2024) · Alzheimer s & Dementia · doi:10.1002/alz.14344 · Cited by 31
Self-citationExperimental modeling of Alzheimer's disease: Translational lessons from cross‐taxon analyses
Yenkoyan, K. B., Kotova, M. M., Apukhtin, K. V., Galstyan, D. S., Amstislavskaya, T. G., Strekalova, T. V., de Abreu, M. S., Chavushyan, V. A., Lim, L. W., Yang, L., et al. (2025) · Alzheimer s & Dementia · doi:10.1002/alz.70273 · Cited by 30
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“Given that the effects of sex and APOE ε4 are known to vary significantly across disease stage and age groups [44, 45], our results should be interpreted within the age range in this cohort.”
Han, W., Zhong-Wen, H., Min, J., Han, Z., Li, W., Yang, L., Fei, L., Lu, H., Ning, Z., & Li, X. (2020) · Applied Microbiology and Biotechnology · doi:10.1007/s00253-020-10894-4 · Cited by 26
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Schilling, L. P., Balthazar, M. L. F., Radanovic, M., Forlenza, O. V., Silagi, M. L., Smid, J., Barbosa, B. J. A. P., Frota, N. A. F., de Souza, L. C., Vale, F. A. C., et al. (2022) · Dementia & Neuropsychologia · doi:10.1590/1980-5764-dn-2022-s102en · Cited by 29
Role of microbial dysbiosis in the pathogenesis of Alzheimer's disease
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Planche, V., & Villain, N. (2023) · JAMA Neurology · doi:10.1001/jamaneurol.2023.0815 · Cited by 26
Nédelec, T., Couvy‐Duchesne, B., Darves‐Bornoz, A., Couronné, R., Monnet, F., Gantzer, L., Lekens, B., Wu, Y., Villain, N., Schrag, A. E., et al. (2023) · Annals of Neurology · doi:10.1002/ana.26670 · Cited by 28
“For AD, accumulation of amyloid can precede a clinical diagnosis of dementia by up to 20 years.(4) Synucleinopathies, including PD and DLB, also have a long prodromal stage, as demonstrated by isolated rapid eye movement (REM) sleep behavioral disorders, which can precede symptomatic PD or DLB by 10 years or more.”
Naimi, N., Seyedmirzaei, H., Hassannejad, Z., & Khaboushan, A. S. (2024) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2024.116691 · Cited by 29
Verberk, I. M. W., Jutte, J., Kingma, M. Y., Vigneswaran, S., Gouda, M., van Engelen, M. E., Alcolea, D. A., Arranz, J., Fortea, J., Lleó, A., et al. (2024) · Alzheimer s & Dementia · doi:10.1002/alz.14088 · Cited by 24
The temporal lobe in typical and atypical Alzheimer disease
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“In patients, amyloid accumulation can be detected 10 years before the onset of clinical symptoms (Vermunt et al., 2019).”
BackgroundChatzikostopoulos, A., Μoraitou, D., Tsolaki, M., Masoura, E. V., Παπαντωνίου, Γ., Sofologi, M., Papaliagkas, V. T., Kougioumtzis, G. Α., & Papatzikis, E. (2022) · Diagnostics · doi:10.3390/diagnostics12071768 · Cited by 28
“For a more precise diagnosis, ADD can be distinguished in mild, moderate, or severe stages [2].”
BackgroundMethodSelf-citationAssociation of tooth count with cognitive decline and dementia in the Finnish adult population
Asher, S., Suominen, A. L., Stephen, R., Ngandu, T., Koskinen, S. V. P., & Solomon, A. (2023) · Journal Of Clinical Periodontology · doi:10.1111/jcpe.13851 · Cited by 25
Meghdadi, A. H., Salat, D. H., Hamilton, J. M., Hong, Y., Boeve, B. F., Louis, E. K. S., Verma, A. K., & Berka, C. (2024) · PLoS ONE · doi:10.1371/journal.pone.0308137 · Cited by 23
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Peripheral inflammation is a potential etiological factor in Alzheimer’s disease
Li, Z., Wang, H., & Yin, Y. (2023) · Reviews in the Neurosciences · doi:10.1515/revneuro-2023-0049 · Cited by 23
Aβ oligomers peak in early stages of Alzheimer's disease preceding tau pathology
Blömeke, L., Rehn, F., Kraemer‐Schulien, V., Kutzsche, J., Pils, M., Bujnicki, T., Lewczuk, P., Kornhuber, J., Freiesleben, S. D., Schneider, L., et al. (2024) · Alzheimer s & Dementia Diagnosis Assessment & Disease Monitoring · doi:10.1002/dad2.12589 · Cited by 26
“Using Spearman correlations and two-sided Mann–Whitney U -tests, we examined the association of oligomer pixel counts with demographic variables and known risk factors for AD, including age, sex, and APOE status, 31,32 as well as associations with further CSF biomarkers.”
MethodVoice-Enabled Intelligent Virtual Agents for People With Amnesia: Systematic Review
Boumans, R., van de Sande, Y., Thill, S., & Bosse, T. (2022) · JMIR Aging · doi:10.2196/32473 · Cited by 23
“For the latter category, the period between first serious cognitive complaints and the diagnosis of dementia can be 10 years and depends on many factors such as age, sex, and general physical premorbid condition [3].”
Cardiometabolic Trajectories Preceding Dementia in Community-Dwelling Older Individuals
Wu, Z., Cribb, L., Wolfe, R. S., Shah, R. C., Orchard, S. G., Owen, A. J., Woods, R. L., Vishwanath, S., Chong, T. T. ‐., Sheets, K. M., et al. (2025) · JAMA Network Open · doi:10.1001/jamanetworkopen.2024.58591 · Cited by 21
Raman Spectroscopy Techniques for the Investigation and Diagnosis of Alzheimer's Disease
Polykretis, P., Banchelli, M., D’Andrea, C., de Angelis, M., & Matteini, P. (2022) · Frontiers in Bioscience-Scholar · doi:10.31083/j.fbs1403022 · Cited by 21
“AD occurs in most cases in subjects over 65, causing memory loss, cognitive decline, progressive impairment of physiological functions and death, usually within 5–12 years from the onset of the symptoms [3].”
BackgroundAlzheimer’s disease is an inherent, natural part of human brain aging: an integrated perspective
Ferrer, I. (2022) · Free Neuropathology · doi:10.17879/freeneuropathology-2022-3806 · Cited by 25
Long, J., Qin, F., Luo, J., Zhong, G., Huang, S., Jing, L., Yi, T., Liu, J., & Jiang, N. (2023) · Bioorganic Chemistry · doi:10.1016/j.bioorg.2023.107026 · Cited by 21
Niotis, K., Saperia, C., Saif, N., Carlton, C., & Isaacson, R. (2024) · Nature Mental Health · doi:10.1038/s44220-023-00191-0 · Cited by 20
Vermunt, L., Dicks, E., Wang, G., Dincer, A., Flores, S. E., Keefe, S., Berman, S., Cash, D. M., Chhatwal, J. P., Cruchaga, C., et al. (2020) · Brain Communications · doi:10.1093/braincomms/fcaa102 · Cited by 20
“A complication when studying sporadic Alzheimer’s disease is the difficulty of placing pre-symptomatic individuals on their disease timeline (Villemagne et al., 2013; Donohue et al., 2014; Young et al., 2014; Roe et al., 2018; Vermunt et al., 2019).”
BackgroundSelf-citationWang, Y., Song, X., Wang, Y., Huang, L., Luo, W., Li, F., Qin, S., Wang, Y., Xiao, J., Wu, Y., et al. (2020) · Critical Reviews in Microbiology · doi:10.1080/1040841x.2020.1794789 · Cited by 23
Sarkar, S., Bhui, U., Kumar, B., Ashique, S., Kumar, P., Sharma, H., Bhowmick, M., Pal, R., & Kumar, T. (2024) · Current Psychiatry Research and Reviews · doi:10.2174/0126660822329981241007105405 · Cited by 25
Zhang, P., Liu, Y., Jin, X., Hu, Z., Yang, J., Lu, H. X., Hang, T., & Song, M. O. (2024) · Journal of Alzheimer s Disease · doi:10.1177/13872877241302498 · Cited by 20
“43 Thus, female mice were selected for this study.”
Caprioglio, C., Garibotto, V., Jessen, F., Frölich, L., Allali, G., Assal, F., Frisoni, G. B., & Altomare, D. (2022) · Journal of Alzheimer s Disease · doi:10.3233/jad-220333 · Cited by 20
An emerging role for stress granules in neurodegenerative disease and hearing loss
Martin, J. L., Dawson, S. J., & Gale, J. E. (2022) · Hearing Research · doi:10.1016/j.heares.2022.108634 · Cited by 23
“Which is significantly shorter than neurodegenerative diseases that do exhibit hearing loss, such as AD, that progress over decades (Vermunt et al., 2019).”
Xing, C., Zhang, X., Wang, D., Chen, H., Gao, X., Sun, C., Guo, W., Roshan, S., Li, Y., Hang, Z., et al. (2024) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2024.08.047 · Cited by 20
Kriit, H. K., Forsberg, B., Åström, D. O., & Oudin, A. (2021) · Environmental Health · doi:10.1186/s12940-021-00750-x · Cited by 21
“For the dementia disease duration, we used an estimate of 6 years, retrieved from a study conducted by Vermunt et al. 2019 [25].”
BackgroundMethodKang, D. W., Wang, S., Um, Y. H., Na, H.-R., Kim, N.-Y., Lee, C. U., & Lim, H. K. (2021) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2021.696735 · Cited by 21
Elhage, A., Cohen, S., Cummings, J. L., van der Flier, W. M., Aisen, P. S. S., Cho, M., Bell, J., & Hampel, H. J. (2024) · Alzheimer s & Dementia · doi:10.1002/alz.14425 · Cited by 21
“14 Based on estimations using patient-level data from six longitudinal cohort studies, the estimated stage-specific duration has substantial ranges: 7.6–13 years in preclinical AD, 4.0–4.6 years in MCI-AD, 2.1–5.0 years in mild AD dementia, and 1.7–6.5 years in moderate to severe AD dementia.”
InfluentialAquino, C. (2021) · Frontiers in Neurology · doi:10.3389/fneur.2021.694329 · Cited by 20
“A study estimated the duration of the pre-clinical phase in ∼10 years, and the prodromal phase in 4–5 years, which corresponds to a window of opportunity to intervene in the biological process of the disease (17).”
BackgroundNeshan, M., Malakouti, S. K., Kamalzadeh, L., Makvand, M., Campbell, A., & Ahangari, G. (2021) · Journal of Alzheimer s Disease · doi:10.3233/jad-210480 · Cited by 19
“In AD, underlying dementia progressively worsens and leads to a disability that generally results in death within 5 to 12 years of onset of symptoms [4].”
Wang, Z., Tan, L., Wang, H.-F., Chen, S., Fu, Y., Gao, P., Ma, Y., Guo, Y., Hou, J., Zhang, D., et al. (2023) · Alzheimer s & Dementia · doi:10.1002/alz.12997 · Cited by 20
Jiménez‐Herrera, R., Contreras, A., Djebari, S., Mulero‐Franco, J., Iborra‐Lázaro, G., Jeremic, D., Navarro‐López, J. D., & Jiménez‐Díaz, L. (2023) · Biology of Sex Differences · doi:10.1186/s13293-023-00545-4 · Cited by 17
Identification ferroptosis-related hub genes and diagnostic model in Alzheimer’s disease
Zhao, H., Wang, J., Li, Z., Wang, S., Yu, G., & Wang, L. (2023) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2023.1280639 · Cited by 20
Mo, H., Kim, J., Kim, J. Y., Kim, J. W., Han, H., Choi, S. H., Rim, Y. A., & Ju, J. H. (2023) · Translational Neurodegeneration · doi:10.1186/s40035-023-00384-8 · Cited by 21
“However, AD has been reported as a multi-factorial disease involving highly phosphorylated tau protein neurofibrillary tangles and the APOE gene [5–7].”
BackgroundSymptoms and conventional treatments of Alzheimer's disease
Chorawala, M. R., Shah, A. C., Pandya, A. J., Kothari, N. R., & Prajapati, B. G. (2024) · Elsevier eBooks · doi:10.1016/b978-0-443-13205-6.00009-1 · Cited by 20
Tariot, P. N., Boada, M., Lanctôt, K. L., Hahn-Pedersen, J. H., Dabbous, F. M., Udayachalerm, S., Rakêt, L. L., Halchenko, Y., Michalak, W., Weidner, W. S., et al. (2024) · Alzheimer s Research & Therapy · doi:10.1186/s13195-024-01399-7 · Cited by 20
“A commonly used estimate of stage-to-stage transition probabilities is based on the Neumann et al. study, which calculated the transition probabilities using the Consortium to Estab-lish a Registry for Alzheimer’s Disease (CERAD) data [22, 23].”
BackgroundMethodInfluentialSensory and motor deficits as contributors to early cognitive impairment
Sayyid, Z. N., Wang, H., Cai, Y., Gross, A. L., Swenor, B. K., Deal, J. A., Lin, F. R., Wanigatunga, A. A., Dougherty, R. J., Tian, Q., et al. (2024) · Alzheimer s & Dementia · doi:10.1002/alz.13715 · Cited by 20
“28,29 To capture this preclinical phase, a classification algo-rithm was recently developed to identify individuals with apparently normal cognition who subsequently progressed to MCI.”
BackgroundInsomnia and risk of all-cause dementia: A systematic review and meta-analysis
Meng, M., Shen, X., Xie, Y., Lan, R., & Zhu, S. (2025) · PLoS ONE · doi:10.1371/journal.pone.0318814 · Cited by 21
Association Between Late-Life Weight Change and Dementia: A Population-based Cohort Study
Guo, J., Marseglia, A., Shang, Y., Dove, A. E., Grande, G., Fratiglioni, L., & Xu, W. (2022) · The Journals of Gerontology Series A · doi:10.1093/gerona/glac157 · Cited by 18
Tomassen, J., den Braber, A., van der Lee, S. J., Reus, L. M., Konijnenberg, E., Carter, S. F., Yaqub, M. M., van Berckel, B. N. M., Collij, L. E., Boomsma, D. I., et al. (2022) · BMC Neurology · doi:10.1186/s12883-022-02925-6 · Cited by 18
Self-citationWhite matter hyperintensity, neurofilament light chain, and cognitive decline
Dhana, A., DeCarli, C. S., Dhana, K., Desai, P., Wilson, R. S., Evans, D. A., & Rajan, K. B. (2022) · Annals of Clinical and Translational Neurology · doi:10.1002/acn3.51720 · Cited by 16
The Effects of Pomegranate Seed Oil on Mild Cognitive Impairment
Chatzikostopoulos, T., Gialaouzidis, M., Koutoupa, A., & Tsolaki, M. (2024) · Journal of Alzheimer s Disease · doi:10.3233/jad-231100 · Cited by 18
Self-citationMoving beyond the prevalent exposure design for causal inference in dementia research
Cribb, L., Moreno‐Betancur, M., Wu, Z., Wolfe, R. S., Pase, M. P., & Ryan, J. L. (2025) · The Lancet Healthy Longevity · doi:10.1016/j.lanhl.2024.100675 · Cited by 19
An Open Question: Is the A2A Adenosine Receptor a Novel Target for Alzheimer’s Disease Treatment?
Merighi, S., Poloni, T. E., Pelloni, L., Pasquini, S., Varani, K., Vincenzi, F., Borea, P. A., & Gessi, S. (2021) · Frontiers in Pharmacology · doi:10.3389/fphar.2021.652455 · Cited by 18
“The early mechanisms leading to Aβ accumulation and initial generation of toxic molecules are elusive and multiple, and belong to the individual trajectory of cerebral aging linked to non-modifiable genetic factors (AD-related polymorphisms, APO-E4 allele, and pathogenic mutations in PSN-1-2 and APP genes, and William…”
BackgroundAn update on Alzheimer's disease: Immunotherapeutic agents, stem cell therapy and gene editing
Patwardhan, A. G., & Belemkar, S. (2021) · Life Sciences · doi:10.1016/j.lfs.2021.119790 · Cited by 19
Vigorous, regular physical exercise may slow disease progression in Alzheimer's disease
Devanand, D. P., Masurkar, A. V., & Wısnıewskı, T. (2023) · Alzheimer s & Dementia · doi:10.1002/alz.12946 · Cited by 18
Nallapu, B. T., Initiative, T. A. D. N., Petersen, K. K., Lipton, R. B., Davatzikos, C. A., & Ezzati, A. (2024) · Journal of Alzheimer s Disease · doi:10.3233/jad-230620 · Cited by 17
“4 allele carriership is associated with a shorter duration of the disease stages [54].”
Lin, H., Sun, Y., Li, M., Zhan, Y., Lin, L., Ding, Z., & Han, Y. (2020) · European Journal of Neurology · doi:10.1111/ene.14226 · Cited by 12
Tu, T., Jiang, J., Zhang, Q., Wan, L., Li, Y., Pan, A., Manavis, J., & Yan, X. (2020) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2020.00093 · Cited by 16
“Stages of Sorfra, Aβ, and pTau Pathogenesis Are Partially Overlapped The clinical course of AD is characterized by progressive memory loss and decline of executive cognitive functions, with neurological dysfunctions occurring at the end disease stage involving failures of sensory, motor, and autonomic functions (McKha…”
BackgroundJin, Y., Zhang, Y., Song, M., Zhou, J., Zhang, H., & Ding, Y. (2026) · Cell Biomaterials · doi:10.1016/j.celbio.2025.100344 · Cited by 17
Vöglein, J., Kostova, I., Arzberger, T., Roeber, S., Schmitz, P., Simons, M., Ruf, V., Windl, O., Herms, J. W., Dieterich, M., et al. (2021) · European Journal of Neurology · doi:10.1111/ene.14800 · Cited by 17
“Several factors that are associated with survival in neurodegenerative diseases have been identified to date, including genetic factors, demographic data and biomarkers in AD [38,39] and FTLD [40– 42] and genetic factors in PSP [43].”
Kapasouri, E. M., Ioannidis, D. C., Cameron, D., Vassiliou, V. S., & Hornberger, M. (2022) · Diagnostics · doi:10.3390/diagnostics12122967 · Cited by 17
“AD is considered a continuum in which earlier asymptomatic stages can be detected on a biological level [5].”
BackgroundBurgelman, M., Dujardin, P., Vandendriessche, C., & Vandenbroucke, R. E. (2023) · Frontiers in Immunology · doi:10.3389/fimmu.2022.1055050 · Cited by 16
“Unfortunately, the identification of early biomarkers is an arduous task as brain changes are estimated to already occur twenty years before symptoms arise (21, 22) together with a large individual variability in starting age, symptoms, and the speed of disease progression.”
BackgroundGarcía-García, A., Rojas, S., & Rodríguez‐Diéguez, A. (2023) · Journal of Materials Chemistry B · doi:10.1039/d3tb00427a · Cited by 16
Prodromal multiple sclerosis: considerations and future utility
Harding, K. E., Kreft, K. L., Ben‐Shlomo, Y., & Robertson, N. P. (2024) · Journal of Neurology · doi:10.1007/s00415-023-12173-4 · Cited by 16
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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