The DOI matches its Crossref record; 47 of the 48 references it cites were found in a registry or an index, and 1 are not checked yet; none of the 38 sources its claims cite is checked for support yet.
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
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
20 Own result · 18 Not checked yet · 10 Own method · 7 Own interpretation
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The study did not reveal significant sex differences in the duration of preclinical and prodromal AD stages.”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > DISCUSSION > Effect of sex
plain- Asserted: passes — The authors put it forward as true.
- 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.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Figure 2A shows for those with preclinical AD a lower predicted overall disease duration at older age, which ranged from 24 years (95% CI, 22-25) at age 60 to 15 years (95% CI, 11-17) at age 80.”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > RESULTS > AD stage duration according to age, sex, and setting
plaincorrelational- Asserted: passes — The authors put it forward as true.
- 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.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“There was no association of baseline abnormal t-tau with the duration of the dementia stages.”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > RESULTS > Tau effect
plain- Asserted: passes — The authors put it forward as true.
- 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.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Figure 2C shows how the total predicted disease duration ranged from 12 to 25 years depending on APOE ε4 genotype, age and setting.”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > RESULTS > APOE effect
plaincorrelational- Asserted: passes — The authors put it forward as true.
- 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.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In 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
plaincorrelational- 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.
In the paper
“The estimation of total disease duration estimates were in some cases longer than the residual life expectancies of population data [46].”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > DISCUSSION > Duration and mortality
What the sources say
- Not checked yetcites [46] www.lifetable.de (2010-2012 USA).
hedged- Asserted: passes — The authors put it forward as true.
- 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.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The duration of preclinical AD at age 70 was shorter in a clinical setting (4 years [95% CI, 3-5]) than in a research setting (11 years [95% CI, 9-13]).”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > RESULTS > AD stage duration according to age, sex, and setting
plaincorrelational- Asserted: passes — The authors put it forward as true.
- 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.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In the 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
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.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Progression to at least one consecutive stage was apparent in 981 (32% of 3,034) participants.”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > RESULTS
plainSingle case- Asserted: passes — The authors put it forward as true.
- 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.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Individuals with preclinical AD and abnormal CSF t-tau showed a trend for an increased progression rate from preclinical to prodromal AD (HR=1.49 [95% CI, 0.95-2.35]).”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > RESULTS > Tau effect
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- 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. 28
- Probably not a substantial claim. 16
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The estimated preclinical AD stage was shortened by around 3 years and the prodromal AD stage by around 2.5 years (Table 3).”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > RESULTS > Tau effect
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- 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.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In prodromal AD, abnormal tau associated with a decreased reversion rate to preclinical AD stage (HR=0.41 [95% CI, 0.23-0.71]) and increased progression rate to the mild AD dementia stage (HR=1.91 [95% CI, 1.48-2.48]).”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > RESULTS > Tau effect
plaincorrelational- Asserted: passes — The authors put it forward as true.
- 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.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Compared to data collected in a research setting, data from clinical settings was associated with a higher progression rate (HR=4.40 [95% CI, 2.80-6.94]) and reversion rate (HR=1.98 [95% CI, 1.15-3.39]) between preclinical and prodromal AD.”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > RESULTS > Transition rates
plaincorrelational- Asserted: passes — The authors put it forward as true.
- 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.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Additionally, in the clinical setting the progression rates from the prodromal AD to the mild AD dementia stage (HR=1.48 [95% CI, 1.34-1.92]) and from the mild AD to the moderate AD dementia stage (HR=1.41 [95% CI,1.16-1.72]) were higher.”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > RESULTS > Transition rates
plaincorrelational- Asserted: passes — The authors put it forward as true.
- 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.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Females had a higher progression rate from mild AD to moderate AD dementia, compared to males (HR=1.24 [95% CI, 1.04-1.47]), while their mortality risk in moderate AD dementia was lower (HR=0.60 [95% CI, 0.46-0.80]).”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > RESULTS > Transition rates
plaincorrelational- Asserted: passes — The authors put it forward as true.
- 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.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The predicted total disease duration, based on the model with age, for an individual with preclinical AD at age 70 was 20 years (95% CI, 17-21), consisting of a preclinical stage of 10 years (95% CI, 8-11), followed by a prodromal stage of 4 years (95% CI, 3-5), mild AD dementia for 3 years (95% CI, 2-3), and moderate AD dementia for 3 years (95% CI, 2-3, Table 2).”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > RESULTS > AD stage duration according to age, sex, and setting
plain- Asserted: passes — The authors put it forward as true.
- 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.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In the clinical setting, for individuals with prodromal AD, the stage duration of prodromal AD was also shorter, and while the dementia stage duration for these individuals was equal between settings, more time was spent in the moderate AD stage (Suppl. table B.7a and b).”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > RESULTS > AD stage duration according to age, sex, and setting
plaincorrelational- Asserted: passes — The authors put it forward as true.
- 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.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Depending on age, sex, APOE genotype, baseline CSF t-tau and setting, the total disease duration varied between 12 and 25 years, the preclinical stage between 2 and 15, the prodromal stage between 3 to 7, mild AD dementia stage between 2 and 6 and moderate AD dementia stage between 1 and 7 years.”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > DISCUSSION
plaincorrelational- Asserted: passes — The authors put it forward as true.
- 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.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“When compared to a non-carrier, an APOE ε4 carrier aged 70 in the clinical setting had a 1.6 years (95% CI, 0.4-3.3; p=0.0295) shorter estimated preclinical AD stage duration, and 1.1 years (95% CI, 0.3-2.1; p=0.0110) shorter prodromal AD stage duration, but 1.0 year (95% CI, 0.3-1.8; p=0.0050) longer mild dementia stage duration (suppl. table B.4).”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > RESULTS > APOE effect
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- 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.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The estimated total duration with starting stage preclinical AD ranged in the clinical setting 19 years (95% CI, 17-20) at age 60 to 11 years (95% CI, 10-12) at age 80 and in the research setting from 26 years (95% CI, 23-28) at age 60 to 15 years (95% CI, 12-17) at age 80.”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > RESULTS > AD stage duration according to age, sex, and setting
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- 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.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“APOE ε4 carriers had, compared to non-carriers, an increased rate of progression from the preclinical AD to prodromal AD stage (HR=1.63 [95% CI, 1.11-2.41]) and from the prodromal AD to mild AD dementia stage (HR=1.50 [95% CI, 1.18-1.90]), and a trend for slower decline from the mild to the moderate AD dementia stage (HR 0.77 [95% CI, 0.60-1.00]).”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > RESULTS > APOE effect
plaindirect- Asserted: passes — The authors put it forward as true.
- 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.
None of the sources cited for this claim have been checked yet.
In the paper
“Unlike previous studies, no effect of tau on mortality and duration of the AD dementia stage were found, which may be explained by dichotomization of CSF t-tau in our analysis [16, 17].”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > DISCUSSION > Effect of tau
What the sources say
- Not checked yetcites [16] Rhodius-Meester HFM,, Disease-related determinants are associated with mortality in dementia due to Alzheimer's disease. Alzheimers Res Ther, 2018 10(1): p. 23. 29458426 PMC5819199
- Not checked yetcites [17] Degerman Gunnarsson M,, High tau levels in cerebrospinal fluid predict nursing home placement and rapid progression in Alzheimer's disease. Alzheimers Res Ther, 2016 8(1): p. 22. 27263933 PMC4893835
hedged- Asserted: passes — The authors put it forward as true.
- 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
“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.
- 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.
None of the sources cited for this claim have been checked yet.
In the paper
“Accumulation of amyloid in the brain is believed to be the first sign of the disease and can precede a clinical diagnosis of dementia by up to 20 years [1, 4, 5].”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > INTRODUCTION
What the sources say
- Not checked yetcites [1] Winblad B,, Defeating Alzheimer's disease and other dementias: a priority for European science and society. Lancet Neurol, 2016 15(5): p. 455– 532. 26987701 source
- Not checked yetcites [4] Jansen WJ,, Prevalence of cerebral amyloid pathology in persons without dementia: a meta-analysis. JAMA, 2015 313(19): p. 1924– 38. 25988462 PMC4486209 source
- Not checked yetcites [5] Jack CR Jr.,, Tracking pathophysiological processes in Alzheimer's disease: an updated hypothetical model of dynamic biomarkers. Lancet Neurol, 2013 12(2): p. 207– 16. 23332364 PMC3622225 source
plainconditional- Asserted: passes — The authors put it forward as true.
- 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.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Age had the strongest effect on the duration of the preclinical and dementia stages, which could be explained by higher progression and mortality rates.”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > DISCUSSION > Effect of age
hedgedconditional- Asserted: passes — The authors put it forward as true.
- 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.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The dementia stage duration was longer in women, which was driven by lower mortality in this group.”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > DISCUSSION > Effect of sex
plaindirect- Asserted: passes — The authors put it forward as true.
- 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
“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.
- 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
“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.
- 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
“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.
- 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.
None of the sources cited for this claim have been checked yet.
In the paper
“The patients with prodromal AD and increased CSF t-tau levels tended to convert sooner to AD dementia [19, 20].”
§ Duration of Preclinical, Prodromal and Dementia Alzheimer Disease Stages in Relation to Age, Sex, and APOE genotype > INTRODUCTION
What the sources say
- Not checked yetcites [19] van Rossum IA,, Injury markers predict time to dementia in subjects with MCI and amyloid pathology. Neurology, 2012 79(17): p. 1809– 16. 23019259 PMC3475623 source
- Not checked yetcites [20] Buchhave P,, Cerebrospinal fluid levels of beta-amyloid 1-42, but not of tau, are fully changed already 5 to 10 years before the onset of Alzheimer dementia. Arch Gen Psychiatry, 2012 69(1): p. 98– 106. 22213792 source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- 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
“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.
- 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
“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.
- 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
“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.
- 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 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
McKhann, G., Drachman, D., Folstein, M., Katzman, R., Price, D., & Stadlan, E. M. (1984) · Neurology · doi:10.1212/wnl.34.7.939 · Cited by 27,915
McKhann, G. M., Knopman, D. S., Chertkow, H., Hyman, B. T., Jack, C. R., Kawas, C. H., Klunk, W. E., Koroshetz, W. J., Manly, J. J., Mayeux, R., et al. (2011) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2011.03.005 · Cited by 18,657
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
Self-citationAlbert, M. S., DeKosky, S. T., Dickson, D., Dubois, B., Feldman, H. H., Fox, N. C., Gamst, A., Holtzman, D. M., Jagust, W. J., Petersen, R. C., et al. (2011) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2011.03.008 · Cited by 10,152 · 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].”
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
Scheltens, P., Blennow, K., Breteler, M. M. B., de Strooper, B., Frisoni, G. B., Salloway, S., & Van der Flier, W. M. (2016) · The Lancet · doi:10.1016/s0140-6736(15)01124-1 · Cited by 3,125
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
Scheltens, P., De Strooper, B., Kivipelto, M., Holstege, H., Chételat, G., Teunissen, C. E., Cummings, J., & van der Flier, W. M. (2021) · The Lancet · doi:10.1016/s0140-6736(20)32205-4 · Cited by 5,465
Self-citationAlzheimer Disease: An Update on Pathobiology and Treatment Strategies
Long, J. M., & Holtzman, D. M. (2019) · Cell · doi:10.1016/j.cell.2019.09.001 · Cited by 3,204
“Dementia due to AD is associated with the onset of significant and progressive disability throughout the disease course with death an inevitable outcome, generally occurring within 5-12 years of symptom onset (Vermunt et al., 2019).”
2023 Alzheimer's disease facts and figures
(2023) · Alzheimer's & Dementia · doi:10.1002/alz.13016 · Cited by 3,212
2024 Alzheimer's disease facts and figures
(2024) · Alzheimer's & Dementia · doi:10.1002/alz.13809 · Cited by 2,536
2020 Alzheimer's disease facts and figures
(2020) · Alzheimer's & Dementia · doi:10.1002/alz.12068 · Cited by 2,353
2022 Alzheimer's disease facts and figures
Anonymous (2022) · Alzheimer s & Dementia · doi:10.1002/alz.12638 · Cited by 2,469
2021 Alzheimer's disease facts and figures
Anonymous (2021) · Alzheimer s & Dementia · doi:10.1002/alz.12328 · Cited by 2,339
Blood-based biomarkers for Alzheimer's disease: towards clinical implementation
Teunissen, C. E., Verberk, I. M. W., Thijssen, E. H., Vermunt, L., Hansson, O., Zetterberg, H., van der Flier, W. M., Mielke, M. M., & del Campo, M. (2022) · The Lancet Neurology · doi:10.1016/s1474-4422(21)00361-6 · Cited by 1,045
“1,4,5 A meta-analysis published in 2016 showed no differences in plasma concentrations of Aβ 1–42 and Aβ 1–40 in individuals with Alzheimer’s disease compared with controls.”
Self-citationGlobal estimates on the number of persons across the Alzheimer's disease continuum
Gustavsson, A., Norton, N., Fast, T., Frölich, L., Georges, J., Holzapfel, D., Kirabali, T., Krolak‐Salmon, P., Rossini, P. M., Ferretti, M. T., et al. (2023) · Alzheimer's & Dementia · doi:10.1002/alz.12694 · Cited by 895
Diagnosis of Early Alzheimer's Disease: Clinical Practice in 2021
Porsteinsson, A. P., Isaacson, R. S., Knox, S., Sabbagh, M. N., & Rubino, I. (2021) · The Journal of Prevention of Alzheimer's Disease · doi:10.14283/jpad.2021.23 · Cited by 744
“The duration of preclinical AD can vary between individuals, but typically lasts 6–10 years depending on the age of onset (10, 11).”
InfluentialAlzheimer’s disease drug development pipeline: 2021
Cummings, J., Lee, G., Zhong, K., Fonseca, J., & Taghva, K. (2021) · Alzheimer's & Dementia: Translational Research & Clinical Interventions · doi:10.1002/trc2.12179 · Cited by 539
2025 Alzheimer's disease facts and figures
(2025) · Alzheimer s & Dementia · doi:10.1002/alz.70235 · Cited by 642
Yin, F. (2023) · The FEBS Journal · doi:10.1111/febs.16344 · Cited by 441
Emerging diagnostics and therapeutics for Alzheimer disease
Self, W. K., & Holtzman, D. M. (2023) · Nature Medicine · doi:10.1038/s41591-023-02505-2 · Cited by 381
Involvement of Lipids in Alzheimer’s Disease Pathology and Potential Therapies
Chew, H., Solomon, V. A., & Fonteh, A. N. (2020) · Frontiers in Physiology · doi:10.3389/fphys.2020.00598 · Cited by 353
Alzheimer’s Disease: An Update and Insights Into Pathophysiology
Abubakar, M. B., Sanusi, K. O., Ugusman, A., Mohamed, W. M. Y., Kamal, H., Ibrahim, N. H., Khoo, C. S., & Kumar, J. (2022) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2022.742408 · Cited by 302
Immunotherapy for Alzheimer’s disease: targeting β-amyloid and beyond
Song, C., Shi, J., Zhang, P., Zhang, Y., Xu, J., Zhao, L., Zhang, R., Wang, H., & Chen, H. (2022) · Translational Neurodegeneration · doi:10.1186/s40035-022-00292-3 · Cited by 266
Pike, K. E., Cavuoto, M. G., Li, L., Wright, B. J., & Kinsella, G. (2021) · Neuropsychology Review · doi:10.1007/s11065-021-09522-3 · Cited by 285
Alzheimer’s pathogenic mechanisms and underlying sex difference
Zhu, D., Montagne, A., & Zhao, Z. (2021) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-021-03830-w · Cited by 275
“The APOE4 has been established as the strongest genetic risk factor for LOAD and related dementia whereas APOE2 is somewhat neuroprotective [5, 13, 15, 20, 23, 29, 31, 92].”
BackgroundPrevention of dementia in an ageing world: Evidence and biological rationale
Grande, G., Qiu, C., & Fratiglioni, L. (2020) · Ageing Research Reviews · doi:10.1016/j.arr.2020.101045 · Cited by 229
Cell type‐specific roles of APOE4 in Alzheimer disease
Blumenfeld, J., Yip, O., Kim, M. J., & Huang, Y. (2024) · Nature Reviews Neuroscience · doi:10.1038/s41583-023-00776-9 · Cited by 202
“Finally, some but not all cases progress to dementia 3–5 .”
The Neuroprotective Potentiality of Flavonoids on Alzheimer’s Disease
Calderaro, A., Patanè, G. T., Tellone, E., Barreca, D., Ficarra, S., Misiti, F., & Laganà, G. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms232314835 · Cited by 208
The Toxicity and Polymorphism of β-Amyloid Oligomers
Huang, Y., & Liu, R. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21124477 · Cited by 176
Recent update on the heterogeneity of the Alzheimer’s disease spectrum
Jellinger, K. A. (2021) · Journal of Neural Transmission · doi:10.1007/s00702-021-02449-2 · Cited by 155
New landscape of the diagnosis of Alzheimer’s disease
Frisoni, G. B., Hansson, O., Nichols, E., Garibotto, V., Schindler, S. E., van der Flier, W. M., Jessen, F., Villain, N., Arenaza-Urquijo, E. M., Crivelli, L., et al. (2025) · The Lancet · doi:10.1016/s0140-6736(25)01294-2 · Cited by 143
Self-citationTao, L., Liu, Q., Zhang, F., Fu, Y., Zhu, X. D., Weng, X., Han, H., Huang, Y., Suo, Y., Chen, L., et al. (2021) · Light Science & Applications · doi:10.1038/s41377-021-00617-3 · Cited by 133
The promise of music therapy for Alzheimer's disease: A review
Matziorinis, A. M., & Koelsch, S. (2022) · Annals of the New York Academy of Sciences · doi:10.1111/nyas.14864 · Cited by 154
Systems-based proteomics to resolve the biology of Alzheimer’s disease beyond amyloid and tau
Rayaprolu, S., Higginbotham, L., Bagchi, P., Watson, C. M., Zhang, T., Levey, A. I., Rangaraju, S., & Seyfried, N. T. (2021) · Neuropsychopharmacology · doi:10.1038/s41386-020-00840-3 · Cited by 118
Dendritic Spines in Alzheimer’s Disease: How the Actin Cytoskeleton Contributes to Synaptic Failure
Pelucchi, S., Stringhi, R., & Marcello, E. E. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21030908 · Cited by 117
Anticholinergic drugs and the risk of dementia: A systematic review and meta-analysis
Zheng, Y., Shi, L., Zhu, X.-M., Bao, Y., Bai, L., Li, J., Liu, J., Han, Y., Shi, J., & Lü, L. (2021) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2021.04.031 · Cited by 122
Chen, Y., Qian, X., Zhang, Y., Su, W., Huang, Y., Wang, X., Chen, X., Zhao, E., Han, L., & Ma, Y. (2022) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2022.840386 · Cited by 119
Alzheimer's disease outlook: controversies and future directions
Frisoni, G. B., Aho, E., Brayne, C., Ciccarelli, O., Dubois, B., Fox, N. C., Frederiksen, K. S., Gabay, C., Garibotto, V., Hofmarcher, T., et al. (2025) · The Lancet · doi:10.1016/s0140-6736(25)01389-3 · Cited by 116
Self-citationPerspectives and challenges in patient stratification in Alzheimer’s disease
Abdelnour, C., Agosta, F., Bozzali, M., Fougère, B., Iwata, A., Nilforooshan, R., Takada, L. T., Viñuela, F., & Traber, M. (2022) · Alzheimer's Research & Therapy · doi:10.1186/s13195-022-01055-y · Cited by 108
Rao, R. V., Subramaniam, K. G., Gregory, J., Bredesen, A. L., Coward, C., Okada, S., Kelly, L., & Bredesen, D. E. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24021659 · Cited by 109
MIND diet and the risk of dementia: a population-based study
de Crom, T. O. E., Mooldijk, S. S., Ikram, M. K., Ikram, M. A., & Voortman, T. (2022) · Alzheimer s Research & Therapy · doi:10.1186/s13195-022-00957-1 · Cited by 105
“6 years, which corresponds largely to the prodromal stage of dementia [14].”
BackgroundNeuroinflammation as a Potential Therapeutic Target in Alzheimer’s Disease
Liu, P., Wang, Y., Sun, Y., & Peng, G. (2022) · Clinical Interventions in Aging · doi:10.2147/cia.s357558 · Cited by 94
“has changed from a traditionally symptom-based disease entity to a clinico-biological construct encompassing a 15–20 year preclinical phase, a 3–6 year prodromal period and a terminal dementia stage.(3) In 2018, the updated National”
BackgroundVisser, P. J., Reus, L. M., Gobom, J., Jansen, I. E., Dicks, E., van der Lee, S. J., Tsolaki, M., Verhey, F. R. J., Popp, J., Martínez‐Lage, P., et al. (2022) · Molecular Neurodegeneration · doi:10.1186/s13024-022-00521-3 · Cited by 92
Self-citationWalker, L. C. (2020) · Free Neuropathology · doi:10.17879/freeneuropathology-2020-3025 · Cited by 113
Ali, A. M., & Kunugi, H. (2020) · Antioxidants · doi:10.3390/antiox9100937 · Cited by 88
APOE-ε4 Carrier Status and Gut Microbiota Dysbiosis in Patients With Alzheimer Disease
Hou, M., Xu, G., Ran, M., Luo, W., & Wang, H. (2021) · Frontiers in Neuroscience · doi:10.3389/fnins.2021.619051 · Cited by 87
“As the effects of age and gender on AD incidence are welldocumented (Fratiglioni et al., 1991; Vermunt et al., 2019), these factors were used as matching variables in this study.”
MethodSadikki, H., Fayossé, A., Cognat, E., Sabia, S., Engelborghs, S., Wallon, D., Alexopoulos, P., Blennow, K., Zetterberg, H., Parnetti, L., et al. (2019) · PLoS Medicine · doi:10.1371/journal.pmed.1003289 · Cited by 87
“Beyond individual genetic susceptibilities, increasing age is the main risk factor of AD [10].”
BackgroundSelf-citationSharoar, M. G., Palko, S., Ge, Y., Saido, T. C., & Yan, R. (2021) · Molecular Neurodegeneration · doi:10.1186/s13024-021-00464-1 · Cited by 78
“The detection of both LAMP1 and hydrolases in DAM may indicate that phagocytic DAM perhaps retain functional lysosomes at later stages of AD development, or even during clinical manifestation [3, 4].”
BackgroundCholesterol Metabolism in Aging and Age-Related Disorders
Saher, G. (2023) · Annual Review of Neuroscience · doi:10.1146/annurev-neuro-091922-034237 · Cited by 88
“The duration of AD stages shortens with age, and aging is the strongest risk factor for AD (DeTure & Dickson 2019, Vermunt et al. 2019).”
BackgroundProdromal Dementia With Lewy Bodies: Clinical Characterization and Predictors of Progression
Beek, M. H. C. T. V., van Steenoven, I., van der Zande, J. J., Barkhof, F., Teunissen, C. E., van der Flier, W. M., & Lemstra, A. W. (2020) · Movement Disorders · doi:10.1002/mds.27997 · Cited by 79
“In Alzheimer’s disease (AD), extensive research has been done on these prodromal stages, usually called mild cognitive impairment (MCI).(6,7) In contrast to MCI as a result of AD (MCI-AD), research on MCI as a result of Lewy bodies (MCI-LB) is limited.”
BackgroundLiposome based drug delivery as a potential treatment option for Alzheimer’s disease
Shukla, S., & Hernandez, C. (2021) · Neural Regeneration Research · doi:10.4103/1673-5374.327328 · Cited by 78
microRNAs as early biomarkers of Alzheimer’s disease: a synaptic perspective
Siedlecki-Wullich, D., Miñano-Molina, A. J., & Rodríguez-Álvarez, J. (2021) · Cells · doi:10.3390/cells10010113 · Cited by 76
“The duration of each phase is not constant but rather depends on the age of onset, gender, and genetic risk factors [5].”
BackgroundLim, D., Tapella, L., Dematteis, G., Genazzani, A. A., Corazzari, M., & Verkhratsky, A. (2023) · Ageing Research Reviews · doi:10.1016/j.arr.2023.101914 · Cited by 75
Lodder, C., Scheyltjens, I., Stancu, I., Lucena, P. B., de Ravé, M. G., Vanherle, S., Vanmierlo, T., Cremers, N., Vanrusselt, H., Brône, B., et al. (2021) · Acta Neuropathologica Communications · doi:10.1186/s40478-021-01204-8 · Cited by 71
“In humans, APOE4 carriers display a higher level of neurodegeneration for a similar level of amyloid pathology [11, 63] and seem to progress faster to more advanced stages of the disease [67].”
BackgroundClinical Trial Endpoints and Their Clinical Meaningfulness in Early Stages of Alzheimer's Disease
Cohen, S., Cummings, J. L., Knox, S., Potashman, M. H., & Harrison, J. (2022) · The Journal of Prevention of Alzheimer s Disease · doi:10.14283/jpad.2022.41 · Cited by 71
“Patients may remain in Stage 3 for ~3–5 years and in Stage 4 for ~3 years, with the individual rate of decline influenced by age, sex, apolipoprotein E (APOE) genotype, and potentially other factors yet to be identified (24).”
BackgroundMelchiorri, D., Merlo, S., Micallef, B., Borg, J.-J., & Dráfi, F. (2023) · Frontiers in Pharmacology · doi:10.3389/fphar.2023.1196413 · Cited by 73
Dysregulated Wnt Signalling in the Alzheimer’s Brain
Aghaizu, N. D., Jin, H., & Whiting, P. J. (2020) · Brain Sciences · doi:10.3390/brainsci10120902 · Cited by 70
Ribarič, S. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23063245 · Cited by 77
The Role of P2X7 Receptor in Alzheimer’s Disease
Francistiová, L., Bianchi, C., Lauro, C. D., Sebastián‐Serrano, Á., de Diego-García, L., Kobolák, J., Dinnyés, A., & Díaz-Hernández, M. (2020) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2020.00094 · Cited by 73
Low-Density Lipoprotein Cholesterol and Alzheimer's Disease: A Systematic Review and Meta-Analysis
Zhou, Z., Liang, Y., Zhang, X., Xu, J., Lin, J., Zhang, R., Kang, K., Liu, C., Zhao, C., & Zhao, M. (2020) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2020.00005 · Cited by 73
Liposomes: An emerging carrier for targeting Alzheimer's and Parkinson's diseases
Pandian, S. R. K., Vijayakumar, K. K., Murugesan, S., & Kunjiappan, S. (2022) · Heliyon · doi:10.1016/j.heliyon.2022.e09575 · Cited by 77
Apolipoprotein E in Alzheimer’s disease trajectories and the next-generation clinical care pathway
Narasimhan, S., Holtzman, D. M., Apostolova, L. G., Cruchaga, C., Masters, C. L., Hardy, J., Villemagne, V. L., Bell, J. S., Cho, M., & Hampel, H. J. (2024) · Nature Neuroscience · doi:10.1038/s41593-024-01669-5 · Cited by 70
“https://doi.org/10.1038/s41593-024-01669-5 have an increased risk of progression to the next stage of the AD con tinuum, while APOE2 carriers have a lower risk of progression 41,42 , prob ably owing to the earlier onset of Aβ pathology 43 .”
InfluentialCacciamani, F., Houot, M., Gagliardi, G. P., Dubois, B., Sikkes, S. A. M., Sánchez‐Benavides, G., Denicolò, E., Molinuevo, J. L., Vannini, P., & Epelbaum, S. (2021) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2021.697234 · Cited by 63
“In a recent study (Vermunt et al., 2019), the preclinical phase lasted on average 10 years, the prodromal phase 4 years, and the dementia phase 6 years, in individuals who presented with preclinical AD at 70 years of age.”
BackgroundSelf-citationSenescence as an Amyloid Cascade: The Amyloid Senescence Hypothesis
Walton, C. C., Begelman, D. V., Nguyen, W., & Andersen, J. K. (2020) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2020.00129 · Cited by 62
Body Mass Index Trajectories Preceding Incident Mild Cognitive Impairment and Dementia
Guo, J., Wang, J., Dove, A., Chen, H., Yuan, C., Bennett, D. A., & Xu, W. (2022) · JAMA Psychiatry · doi:10.1001/jamapsychiatry.2022.3446 · Cited by 62
Mishra, P., Silva, A., Sharma, J., Nguyen, J., Pizzo, D. P., Hinz, D., Sahoo, D., & Cherqui, S. (2023) · Cell Reports · doi:10.1016/j.celrep.2023.112956 · Cited by 64
Alzheimer’s disease beyond amyloid: strategies for future therapeutic interventions
Shi, J., Sabbagh, M. N., & Vellas, B. J. (2020) · BMJ · doi:10.1136/bmj.m3684 · Cited by 62
Alzheimer’s disease and drug delivery across the blood–brain barrier: approaches and challenges
Iqbal, I., Saqib, F., Mubarak, Z., Latif, M. F., Wahid, M., Nasir, B., Shahzad, H., Sharifi-Rad, J., & Mubarak, M. S. (2024) · European Journal of Medical Research · doi:10.1186/s40001-024-01915-3 · Cited by 60
“The phases of dementia are characterized as mild, moderate, and severe dementia, which represent the extent to which symptoms impair one’s capacity to carry out daily activities [38].”
BackgroundXi, Y., Zhang, Y., Zhou, Y., Liu, Q., Chen, X., Liu, X., Grune, T., Shi, L. S., Hou, M., & Liu, Z. (2022) · Redox Biology · doi:10.1016/j.redox.2022.102595 · Cited by 62
Dubbelman, M. A., Jutten, R. J., Farias, S. T., Amariglio, R. E., Buckley, R. F., Visser, P. J., Rentz, D. M., Johnson, K. A., Properzi, M. J., Schultz, A. P., et al. (2020) · Alzheimer s Research & Therapy · doi:10.1186/s13195-020-00706-2 · Cited by 70
Self-citationAlzheimer’s disease: a review on the current trends of the effective diagnosis and therapeutics
Manap, A. S. A., Almadodi, R., Sultana, S., Sebastian, M. G., Kavani, K. S., Lyenouq, V. E., & Shankar, A. (2024) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2024.1429211 · Cited by 66
Mechanisms of neurodegeneration — Insights from familial Alzheimer’s disease
Chávez‐Gutiérrez, L., & Szaruga, M. (2020) · Seminars in Cell and Developmental Biology · doi:10.1016/j.semcdb.2020.03.005 · Cited by 59
Predicted Lifetime Health Outcomes for Aducanumab in Patients with Early Alzheimer’s Disease
Herring, W. L., Gould, I. G., Fillit, H. M., Lindgren, P., Forrestal, F., Thompson, R., & Pemberton-Ross, P. J. (2021) · Neurology and Therapy · doi:10.1007/s40120-021-00273-0 · Cited by 57
Jack, C. R., Therneau, T. M., Lundt, E. S., Wiste, H. J., Mielke, M. M., Knopman, D. S., Graff‐Radford, J., Lowe, V. J., Vemuri, P., Schwarz, C. G., et al. (2022) · Brain Communications · doi:10.1093/braincomms/fcac017 · Cited by 59
The Burden of Alzheimer’s Disease Mortality in the United States, 1999-2018
Zhao, X., Li, C., Ding, G., Heng, Y., Li, A., Wang, W., Hou, H., Wen, J., & Zhang, Y. (2021) · Journal of Alzheimer s Disease · doi:10.3233/jad-210225 · Cited by 55
“As evidenced by numerous studies, AD develops gradually [26, 27].”
Cell Membrane Biomimetic Nanoparticles with Potential in Treatment of Alzheimer’s Disease
Zhong, X., Na, Y., Yin, S., Yan, C., Gu, J., Zhang, N., & Geng, F. (2023) · Molecules · doi:10.3390/molecules28052336 · Cited by 54
“The possible predisposing factor of dementia in elder citizens is neuronal loss and cognitive impairment brought on by buildup of aggregation of amyloid-β (Aβ) and intracellular neurofibrillary tangles with aging [2].”
BackgroundDiagnostic Accuracy of Blood-Based Biomarker Panels: A Systematic Review
Hardy-Sosa, A., León‐Arcia, K., Llibre‐Guerra, J. J., Berlanga‐Acosta, J., Baez, S. D. L. C., Guillén, G. E., & Valdes-Sosa, P. A. (2022) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2022.683689 · Cited by 57
NAKAI, T., Yamada, K., & Mizoguchi, H. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22115549 · Cited by 53
“The length of each phase is affected by the patient’s age, genetics, gender, and other factors [6].”
BackgroundYuan, J., Maserejian, N. N., Liu, Y., Devine, S., Gillis, C., Massaro, J. M., & Au, R. (2020) · Journal of Alzheimer s Disease · doi:10.3233/jad-200786 · Cited by 47
Inflammatory bowel disease: A potential pathogenic factor of Alzheimer's disease
Wang, D., Zhang, X., & Du, H. (2022) · Progress in Neuro-Psychopharmacology and Biological Psychiatry · doi:10.1016/j.pnpbp.2022.110610 · Cited by 52
Zhao, Z., Liu, Y., Ruan, S., & Hu, Y. (2023) · International Journal of Nanomedicine · doi:10.2147/ijn.s444115 · Cited by 49
The Neuroprotective and Neurodegeneration Effects of Heme Oxygenase-1 in Alzheimer’s Disease
Si, Z., & Wang, X. (2020) · Journal of Alzheimer s Disease · doi:10.3233/jad-200720 · Cited by 46
Mechanistic and therapeutic role of NLRP3 inflammasome in the pathogenesis of Alzheimer's disease
Jha, D., Bakker, E. N. T. P., & Kumar, R. K. (2023) · Journal of Neurochemistry · doi:10.1111/jnc.15788 · Cited by 48
Gut microbiome and Alzheimer’s disease: What we know and what remains to be explored
Kapoor, B., Biswas, P., Gulati, M., Rani, P., & Gupta, R. (2024) · Ageing Research Reviews · doi:10.1016/j.arr.2024.102570 · Cited by 46
Arslan, B., Brum, W. S., Pola, I., Therriault, J., Rahmouni, N., Stevenson, J., Servaes, S., Tan, K., Vitali, P., Montembeault, M., et al. (2025) · Alzheimer s Research & Therapy · doi:10.1186/s13195-025-01692-z · Cited by 61
Self-citationWang, L., Shui, X., Diao, Y., Chen, D., Zhou, Y., & Lee, T. H. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms242216259 · Cited by 49
“One explanation for numerous failed clinical trials might be that the neuropathological alterations of AD start 10–20 years before detectable clinical onset [184,185].”
BackgroundNeuroprotective Roles of the Reverse Transsulfuration Pathway in Alzheimer’s Disease
Paul, B. D. (2021) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2021.659402 · Cited by 42
“The disease has a long prodromal and preclinical phase, and it may take years for symptoms to manifest, the most noticeable of which include memory impairments and language difficulties (Bateman et al., 2012; Villemagne et al., 2013; Vermunt et al., 2019).”
BackgroundMonoclonal Antibody Therapy in Alzheimer’s Disease
Neațu, M., Covaliu, A., Ioniță, I., Jugurt, A., Davidescu, E. I., & Popescu, B. O. (2023) · Pharmaceutics · doi:10.3390/pharmaceutics16010060 · Cited by 46
“…(MCI) caused by Alzheimer’s disease, and Alzheimer’s dementia, which includes stages of mild, moderate, and severe dementia (Figure 1) [61,62,65]. disease, mild cognitive impairment (MCI) caused by Alzheimer’s disease, and Alzheimer’s dementia, which includes stages of mild, moderate,…”
BackgroundInfluentialIncidence of Mild Cognitive Impairment, Conversion to Probable Dementia, and Mortality
Zhang, Y., Natale, G., & Clouston, S. (2021) · American Journal of Alzheimer s Disease & Other Dementias® · doi:10.1177/15333175211012235 · Cited by 43
Wang, K., & Liu, H. (2021) · Regional Anesthesia & Pain Medicine · doi:10.1136/rapm-2021-102733 · Cited by 47
Ketones: potential to achieve brain energy rescue and sustain cognitive health during ageing
Myette‐Côté, É., Soto-Mota, A., & Cunnane, S. C. (2021) · British Journal Of Nutrition · doi:10.1017/s0007114521003883 · Cited by 44
“ologies can be present over 20 years before the onset of clinical symptoms(23) which offers a critical window of opportunity to ini-”
BackgroundSpeech and language processing with deep learning for dementia diagnosis: A systematic review
Shi, M., Cheung, G., & Shahamiri, S. R. (2023) · Psychiatry Research · doi:10.1016/j.psychres.2023.115538 · Cited by 46
Linking activity dyshomeostasis and sleep disturbances in Alzheimer disease
Slutsky, I. (2024) · Nature reviews. Neuroscience · doi:10.1038/s41583-024-00797-y · Cited by 43
“Thus, most individuals with MCI remain stable, or even revert to normal cognition 2 .”
Eggenberger, P., Bürgisser, M., Rossi, R. M., & Annaheim, S. (2021) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2021.585904 · Cited by 44
2026 Alzheimer's disease facts and figures
(2026) · Alzheimer s & Dementia · doi:10.1002/alz.71345 · Cited by 69
Mechanistic and therapeutic role of Drp1 in the pathogenesis of Alzheimer's disease
Bera, A., Lavanya, G., Reshmi, R., Dev, K., & Kumar, R. K. (2022) · European Journal of Neuroscience · doi:10.1111/ejn.15611 · Cited by 43
The vascular contribution of apolipoprotein E to Alzheimer’s disease
Chen, F., Zhao, J., Meng, F., He, F., Ni, J., & Fu, Y. (2024) · Brain · doi:10.1093/brain/awae156 · Cited by 39
The association between insomnia and cognitive decline: A scoping review
Zhang, X., Yin, J., Sun, X., Qu, Z., Zhang, J., & Zhang, H. (2024) · Sleep Medicine · doi:10.1016/j.sleep.2024.10.021 · Cited by 42
Avelar‐Pereira, B., Belloy, M. E., O'Hara, R. M., Hosseini, S. M. H., & Initiative, A. D. N. (2022) · Molecular Psychiatry · doi:10.1038/s41380-022-01886-z · Cited by 42
“Participants were considered AD if they met the NINCDS-ADRDA criteria for probable AD [45, 46].”
MethodKetone bodies mediate alterations in brain energy metabolism and biomarkers of Alzheimer’s disease
Ramezani, M., Fernando, M. G., Eslick, S., Asih, P. R., Shadfar, S., Bandara, E. M. S., Hillebrandt, H., Meghwar, S., Shahriari, M., Chatterjee, P., et al. (2023) · Frontiers in Neuroscience · doi:10.3389/fnins.2023.1297984 · Cited by 39
“…phase of AD referring to the mild cognitive impairment (MCI) with an impairment in at least one cognitive domain (Douglas and Scharre, 2019; Vermunt et al., 2022), and severe AD dementia or symptomatic AD is the late-stage AD characterized by a progressive functional impairments, and more…”
BackgroundTau protein profiling in tauopathies: a human brain study
Lantero‐Rodriguez, J., Camporesi, E., Montoliu‐Gaya, L., Gobom, J., Piotrowska, D., Olsson, M., Matečko‐Burmann, I., Becker, B., Brinkmalm, A., Burmann, B. M., et al. (2024) · Molecular Neurodegeneration · doi:10.1186/s13024-024-00741-9 · Cited by 42
“Additionally, sporadic AD is a comparatively slow progressing disease, presenting a total disease duration (including preclinical AD) between 12 and 25 years [62], contrasting with PSP and CBD, which are all characterized by a faster progression [63, 64].”
BackgroundSelf-citationBirkenbihl, C., Salimi, Y., Fröhlich, H., Initiative, F. T. J. A. D. N., & Initiative, T. A. D. N. (2021) · Alzheimer s & Dementia · doi:10.1002/alz.12387 · Cited by 39
Self-citationDulewicz, M., Kulczyńska‐Przybik, A., Mroczko, P., Kornhuber, J., Lewczuk, P., & Mroczko, B. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23158598 · Cited by 38
“noted, the estimation of disease duration becomes more accurate if age, sex, clinical status, APOE and abnormal Tau in CSF are included [77].”
BackgroundLipids and brain inflammation in APOE4-associated dementia
Duro, M. V. V., Ebright, B., & Yassine, H. N. (2021) · Current Opinion in Lipidology · doi:10.1097/mol.0000000000000801 · Cited by 39
“There is a long preclinical phase in AD lasting decades and is characterized by amyloid accumulation in the brain and subtle cognitive changes [69].”
BackgroundDissociable effects of APOE ε4 and β-amyloid pathology on visual working memory
Lu, K., Nicholas, J. M., Pertzov, Y., Grogan, J. P., Masud Husain, B., Pavisic, I. M., James, S., Parker, T. D., Lane, C., Keshavan, A., et al. (2021) · Nature Aging · doi:10.1038/s43587-021-00117-4 · Cited by 36
Oumata, N., Lu, K., Teng, Y., Cavé, C., Yu, P., Galons, H., & Roques, B. P. (2022) · European Journal of Medicinal Chemistry · doi:10.1016/j.ejmech.2022.114578 · Cited by 36
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 ›
Are you an author, or do you see a problem with this page? Request a review
