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Preclinical Alzheimer's disease and its outcome: a longitudinal cohort study
Open accessAbstract
Background New research criteria for preclinical Alzheimer's disease have been proposed, which include stages for cognitively normal individuals with abnormal amyloid markers (stage 1), abnormal amyloid and neuronal injury markers (stage 2), or abnormal amyloid and neuronal injury markers and subtle cognitive changes (stage 3). We aimed to investigate the prevalence and long-term outcome of preclinical Alzheimer's disease according to these criteria.Methods Participants were cognitively normal (clinical dementia rating [CDR]=0) community-dwelling volunteers aged at least 65 years who were enrolled between 1998 and 2011 at the Washington University School of Medicine (MO, USA). CSF amyloid-β1-42 and tau concentrations and a memory composite score were used to classify participants as normal (both markers normal), preclinical Alzheimer's disease stage 1-3, or suspected non-Alzheimer pathophysiology (SNAP, abnormal injury marker without abnormal amyloid marker). The primary outcome was the proportion of participants in each preclinical AD stage. Secondary outcomes included progression to CDR at least 0·5, symptomatic Alzheimer's disease (score of at least 0·5 for memory and at least one other domain and cognitive impairments deemed to be due to Alzheimer's disease), and mortality. We undertook survival analyses using subdistribution and standard Cox hazards models and linear mixed models.Findings Of 311 participants, 129 (41%) were classed as normal, 47 (15%) as stage 1, 36 (12%) as stage 2, 13 (4%) as stage 3, 72 (23%) as SNAP, and 14 (5%) remained unclassified. The 5-year progression rate to CDR at least 0·5, symptomatic Alzheimer's disease was 2% for participants classed as normal, 11% for stage 1, 26% for stage 2, 56% for stage 3, and 5% for SNAP. Compared with individuals classed as normal, participants with preclinical Alzheimer's disease had an increased risk of death after adjusting for covariates (hazard ratio 6·2, 95% CI 1·1-35·0; p=0·040).Interpretation Preclinical Alzheimer's disease is common in cognitively normal elderly people and is associated with future cognitive decline and mortality. Thus, preclinical Alzheimer's disease could be an important target for therapeutic intervention.Funding National Institute of Aging of the National Institutes of Health (P01-AG003991, P50-AG05681, P01-AG02676), Internationale Stichting Alzheimer Onderzoek, the Center for Translational Molecular Medicine project LeARN, the EU/EFPIA Innovative Medicines Initiative Joint Undertaking, and the Charles and Joanne Knight Alzheimer Research Initiative.
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“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].”
From Duration of preclinical, prodromal, and dementia stages of Alzheimer's disease in relation to age, sex, and APOE genotype (2019) · cites this paper as [12]
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“Initial studies in this emerging area have identified subgroups of older adults with subtle cognitive decline that do not conform to expected patterns and investigators have designated them as Suspected Non-Alzheimer Pathology (SNAP) and Unclassified groups [51, 52].”
From Neuropsychological Criteria for Mild Cognitive Impairment Improves Diagnostic Precision, Biomarker Associations, and Progression Rates (2014) · cites this paper as [52]
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“The rate of cognitive decline is significantly greater for cognitively impaired and CU individuals who have abnormalities in both an amyloid biomarker and a second biomarker type (which could be CSF T-tau or P-tau, atrophy, or hypometabolism) in comparison to individuals who have neither or only one of these biomarker abnormalities [30–35,39,40,42–45].”
From NIA‐AA Research Framework: Toward a biological definition of Alzheimer's disease (2018) · cites this paper as [32]
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“However, the combination of an abnormal MRI, CSF T-tau, or FDG PET study with an abnormal amyloid biomarker provides much more powerful prediction of future cognitive decline [30–35,39,40,42–45] than an abnormal amyloid study alone.”
From NIA‐AA Research Framework: Toward a biological definition of Alzheimer's disease (2018) · cites this paper as [32]
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“longitudinal studies have demonstrated that soluble p-tau and t-tau are increased already in preclinical disease (e.g., no cognitive impairment but evidence of AD pathology).5,6”
From Cerebrospinal fluid p-tau231 as an early indicator of emerging pathology in Alzheimer's disease (2022) · cites this paper as [5]
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BackgroundApplication of the IWG-2 Diagnostic Criteria for Alzheimer’s Disease to the ADNI
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BackgroundAmyloid‐β, cortical thickness, and subsequent cognitive decline in cognitively normal oldest‐old
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Biomarkers and Tools for Predicting Alzheimer's Disease in the Preclinical Stage
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“At the behavioral level, previous results have reported that the t-tau/Aβ42 ratio is more predictive of imminent cognitive decline in CN older adults than either t-tau or Aβ42 individually (Fagan et al., 2007; Vos et al., 2013).”
Estimates of age-related memory decline are inflated by unrecognized Alzheimer's disease
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“The specificity of these AD tau biomarkers may improve the prediction of the risk of cognitive decline in individuals who ultimately progress to clinical AD (18).”
BackgroundCSF total tau as a proxy of synaptic degeneration
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InfluentialCerebrovascular disease in suspected non‐Alzheimer's pathophysiology and cognitive decline over time
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Self-citationWeighting and standardization of frequencies to determine prevalence of AD imaging biomarkers
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“In contrast, one study among CN participants reported a lower frequency of A2N1 in men vs women based on CSF b-amyloid and tau.(29) The prevalence estimates for A/N categories are also consistent with our unadjusted estimates of frequencies previously reported among a smaller sample of CN MCSA participants.”
ResultNeuroimaging of Diseases Causing Dementia
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“positive), neglecting the fact that the NIA–AA guidelines also consider borderline biomarker values, and that in many cases biomarker values are in fact neither clearly positive nor negative [2, 11].”
BackgroundUnderlying Biological Processes in Mild Cognitive Impairment: Amyloidosis Versus Neurodegeneration
Santana, I. J., Baldeiras, I., Santiago, B., Duro, D., Freitas, S., Tábuas‐Pereira, M., Almeida, M. R., & Oliveira, C. R. (2018) · Journal of Alzheimer s Disease · doi:10.3233/jad-179908 · Cited by 15
“This unexpected high prevalence of the SNAP group has been confirmed in studies with preclinical forms [15, 16] as well as in MCI stage [13] and remarkably, this last large MCI multicenter study, also showed that the 3-year progression rate to Alzheimer-type dementia was as high in the SNAP group…”
Brain Amyloid Pathology and Cognitive Function
Visser, P. J., & Tijms, B. M. (2017) · JAMA · doi:10.1001/jama.2017.6895 · Cited by 15
Self-citationLi, Q., Hu, H., Zhang, G.-W., Hu, H., Ou, Y., Huang, L., Wang, A.-Y., Gao, P., Ma, L., Tan, L., et al. (2024) · Alzheimer s Research & Therapy · doi:10.1186/s13195-024-01396-w · Cited by 15
Wen, Q., Wittens, M. M. J., Engelborghs, S., van Herwijnen, M. H. M., Tsamou, M., Roggen, E., Smeets, H. J. M., Krauskopf, J., & Briedé, J. J. (2024) · ACS Chemical Neuroscience · doi:10.1021/acschemneuro.3c00740 · Cited by 14
Decoding molecular mechanisms: brain aging and Alzheimer’s disease
Hayat, M., Syed, R. A., Qaiser, H., Uzair, M., Al-Regaiey, K., Khallaf, R. A., Albassam, L. A. M., Kaleem, I., Wang, X., Wang, R., et al. (2024) · Neural Regeneration Research · doi:10.4103/nrr.nrr-d-23-01403 · Cited by 14
Antoniades, M., Srinivasan, D., Wen, J., Erus, G., Abdulkadir, A., Mamourian, E., Melhem, R., Hwang, G., Cui, Y., Govindarajan, S. T., et al. (2024) · EBioMedicine · doi:10.1016/j.ebiom.2024.105399 · Cited by 13
“50 Similarly, although amyloid positivity increases with age in persons without dementia, it is consistently higher in cognitively normal individuals and MCI who are APOE-ε 4 carriers.”
BackgroundSelf-citationNetwork dysfunction in cognitively normal APOE ε4 carriers is related to subclinical tau
Butt, O. H., Meeker, K. L., Wisch, J. K., Schindler, S. E., Fagan, A. M., Benzinger, T. L. S., Cruchaga, C., Holtzman, D. M., Morris, J. C., & Ances, B. M. (2021) · Alzheimer s & Dementia · doi:10.1002/alz.12375 · Cited by 12
Self-citationMa, L., Chen, J., Wang, R., Han, Y., Zhang, J., Dong, W., Zhao, Z., Liu, Y., & Chu, X. (2014) · Journal of Clinical Neuroscience · doi:10.1016/j.jocn.2014.04.028 · Cited by 14
“Alzheimer’s disease (AD) is an age-related chronic degenerative disease that damages the nervous system, but its etiology is still unknown [1,2].”
Hohman, T. J., Dumitrescu, L. C., Oksol, A., Wagener, M. A., Gifford, K. A., Jefferson, A. L., & Initiative, A. D. N. (2017) · PLoS ONE · doi:10.1371/journal.pone.0188501 · Cited by 15
Butterfield, D. A. (2018) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2018.08.035 · Cited by 13
“Preclinical AD is a relatively newly recognized stage of AD [15].”
BackgroundAnti-Correlated Cerebrospinal Fluid Biomarker Trajectories in Preclinical Alzheimer’s Disease
Gomar, J. J., Conejero-Goldberg, C., Davies, P., Goldberg, T. E., & Initiative, F. T. A. D. N. (2016) · Journal of Alzheimer’s Disease · doi:10.3233/jad-150937 · Cited by 13
“Findings that a group of CI subjects had CSF tau but not amyloid abnormalities were consistent with this view [6].”
ResultHassenstab, J. J., Nicosia, J., LaRose, M., Aschenbrenner, A. J., Gordon, B. A., Benzinger, T. L. S., Xiong, C., & Morris, J. C. (2021) · Alzheimer s Research & Therapy · doi:10.1186/s13195-021-00894-5 · Cited by 13
“Of particular importance, especially for studies that enroll large asymptomatic cohorts, is that the tests included are sensitive enough to detect subtle changes in cognition that characterize the preclinical asymptomatic stages of AD [1, 2].”
BackgroundResultSelf-citationInsights into cognitive aging and Alzheimer’s disease using amyloid PET and structural MRI scans
Duara, R., Barker, W., Loewenstein, D., Greig, M. T., Rodriguez, R. A., Goryawala, M., Zhou, Q., & Adjouadi, M. (2015) · Clinical and Translational Imaging · doi:10.1007/s40336-015-0110-6 · Cited by 15
“Subjects who have been labeled as SNAP have been more frequently found to be e4-negative and 28 % of these individuals subsequently become amyloid positive within a span of 2–3 years [89].”
BackgroundGrilli, M. D., Knoff, A. A. W., Huentelman, M. J., & Ryan, L. (2021) · Journal of the International Neuropsychological Society · doi:10.1017/s1355617720001319 · Cited by 14
“Alzheimer’s disease (AD) causes a protracted period of pathological changes that may begin years before a clinical diagnosis of cognitive impairment (Jack et al., 2013; Sperling et al., 2011; Vos et al., 2013).”
BackgroundUndetected Neurodegenerative Disease Biases Estimates of Cognitive Change in Older Adults
Harrington, K., Aschenbrenner, A. J., Maruff, P. T., Masters, C. L., Fagan, A. M., Benzinger, T. L. S., Gordon, B. A., Cruchaga, C., Morris, J. C., & Hassenstab, J. J. (2021) · Psychological Science · doi:10.1177/0956797620985518 · Cited by 12
Self-citationShen, X., Kuo, K., Yang, Y., Li, H., Chen, S., Cui, M., Tan, L., Dong, Q., Yu, J., & Initiative, A. D. N. (2021) · Alzheimer s & Dementia Diagnosis Assessment & Disease Monitoring · doi:10.1002/dad2.12198 · Cited by 13
Low Subicular Volume as an Indicator of Dementia-Risk Susceptibility in Old Age
Kagerer, S. M., Schroeder, C., Bergen, J. M. G. V., Schreiner, S. J., Meyer, R., Steininger, S. C., Vionnet, L., Gietl, A. F., Treyer, V., Buck, A., et al. (2022) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2022.811146 · Cited by 14
Alm, K. H., Faria, A. V., Moghekar, A., Pettigrew, C. A., Soldan, A., Mori, S., Albert, M., & Bakker, A. (2019) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2019.11.011 · Cited by 13
“Recent evidence indicates that CSF AD biomarkers predict longitudinal cognitive decline among cognitively normal individuals (Soldan et al., 2016; Vos et al., 2013), as well as progression to MCI (Moghekar et al.”
BackgroundUltra-Early Phase pathologies of Alzheimer’s disease and other neurodegenerative diseases
Okazawa, H. (2017) · Proceedings of the Japan Academy Series B · doi:10.2183/pjab.93.022 · Cited by 12
Spencer, B. E., Jennings, R. G., Brewer, J. B., & Initiative, A. D. N. (2019) · Journal of Alzheimer s Disease · doi:10.3233/jad-181243 · Cited by 15
“Longitudi-nalstudiesofunimpairedindividualsdemonstrated that amyloid positivity may appear years before clinically relevant decline [4] and does not predict decline as well alone as it does in combination with abnormal tau [5, 6], suggesting a benefit to evaluating multiple biomarkers.”
Clinical trials in Alzheimer's disease
Delrieu, J., & Vellas, B. J. (2015) · Wiley eBooks · doi:10.1002/9781118323434.ch9 · Cited by 13
Roe, C., Babulal, G., Mishra, S., Gordon, B., Stout, S. H., Ott, B. L., Carr, D., Ances, B., Morris, J., & Benzinger, T. (2017) · Journal of Alzheimer's Disease · doi:10.3233/jad-170521 · Cited by 15
Self-citationDistribution of Cerebrospinal Fluid Biomarker Profiles in Patients Explored for Cognitive Disorders
Paquet, C., Bouaziz-Amar, É., Cognat, E., Volpe‐Gillot, L., Haddad, V., Mahieux, F., Dekimeche, S., Defontaines, B., Chabriat, H., Belin, C., et al. (2018) · Journal of Alzheimer s Disease · doi:10.3233/jad-180240 · Cited by 13
The landscape of ageing—insights from AD imaging markers
Villemagne, V. L., & Masters, C. L. (2014) · Nature Reviews Neurology · doi:10.1038/nrneurol.2014.214 · Cited by 12
The prognostic value of ATN Alzheimer biomarker profiles in cognitively normal individuals
Vos, S. J. B., & Duara, R. (2019) · Neurology · doi:10.1212/wnl.0000000000007223 · Cited by 12
“In this preclinical stage, biomarkers of amyloid pathology and neurodegeneration have prognostic value with regard to cognitive outcome.(1,2) The newly proposed ATN classification framework aims to further refine the pathophysiology and staging of AD, by differentiating between several neurodegeneration markers (T and…”
BackgroundSelf-citationPredicting Driving Cessation Among Cognitively Normal Older Drivers
Babulal, G. M., Chen, L., Murphy, S. A., Carr, D. B., & Morris, J. C. (2024) · Neurology · doi:10.1212/wnl.0000000000209426 · Cited by 11
Self-citationKoberskaya, N. N. (2019) · Neurology neuropsychiatry Psychosomatics · doi:10.14412/2074-2711-2019-3s-52-60 · Cited by 12
Defining Amyloid Pathology in Persons With and Without Dementia Syndromes
Rosenberg, R. N. (2015) · JAMA · doi:10.1001/jama.2015.5361 · Cited by 11
Wang, J., Ackley, S. F., Woodworth, D. C., Sajjadi, S. A., DeCarli, C. S., Fletcher, E. M., Glymour, M. M., Jiang, L., Kawas, C. H., & Corrada, M. M. (2024) · Neurology · doi:10.1212/wnl.0000000000209665 · Cited by 10
APOE ɛ4 Genotype, Amyloid, and Clinical Disease Progression in Cognitively Normal Older Adults
Hollands, S., Lim, Y. Y., Laws, S. M., Villemagne, V. L., Pietrzak, R. H., Harrington, K., Porter, T., Snyder, P. J., Ames, D. J., Fowler, C. J., et al. (2017) · Journal of Alzheimer s Disease · doi:10.3233/jad-161019 · Cited by 11
“+, (cid:2) 4 carriage is not associated with cognitive decline [22, 23].”
Alzheimer’s Disease (AD): Risks, Treatments, Prevention, and Future Implementations
Huma, T., Nawaz, R., Li, X., & Willden, A. (2022) · Advances in Alzheimer s Disease · doi:10.4236/aad.2022.112002 · Cited by 11
“The first, Stage 1 [Mild] can last 2 - 4 years [7].”
BackgroundCaballero, M. Á. A., Initiative, A. D. N., Klöppel, S., Dichgans, M., & Ewers, M. (2016) · Journal of Alzheimer s Disease · doi:10.3233/jad-160327 · Cited by 10
“Those brain areas have previously been shown to support higher cognitive functions such as episodic memory and executive function, which are affected by aging and show accelerated decline early in the course of AD [4, 15, 16].”
BackgroundChung, J. K., Initiative, A. D. N., Plitman, E., Nakajima, S., Caravaggio, F., Iwata, Y., Gerretsen, P., Kim, J., Takeuchi, H., Shinagawa, S., et al. (2017) · Journal of Alzheimer s Disease · doi:10.3233/jad-170201 · Cited by 11
“However, some studies provide evidence supportive of the role of A role in promoting cognitive decline; A groups (A +ND+ and A +ND–) [11] and an A +ND+ group from healthy elderly individuals show progressive cognitive deterioration [4], while SNAP and A –ND– groups from cognitively normal elderly population show compa…”
Amyloid-β — a reflection of risk or a preclinical marker?
Jack, C. R., & Vemuri, P. (2018) · Nature Reviews Neurology · doi:10.1038/s41582-018-0008-9 · Cited by 10
Preclinical Alzheimer’s Disease: Implications for Refinement of the Concept
Vos, S. J. B., & Visser, P. J. (2018) · Journal of Alzheimer s Disease · doi:10.3233/jad-179943 · Cited by 12
“, 2013 [2] after 5 y after 5 y after 5 y after 5 y Ref HR = 4.”
BackgroundSelf-citationLv, S., Zhou, X., Li, Y., Zhang, S., Wang, Y., Jia, S., Niu, X., Wang, L., & Peng, D. (2021) · Medical Science Monitor · doi:10.12659/msm.932998 · Cited by 9
“A study showed that normal elderly individuals with ApoE e4 homozygotes (e4/e4) have a very high risk of developing clinical AD [17].”
BackgroundResultAguilar-Navarro, S. G., Mimenza-Alvarado, A. J., Ávila‐Funes, J. A., Juárez‐Cedillo, T., Bernal‐López, C., & Hernández‐Favela, C. G. (2017) · Revista de investigaci�n Cl�nica · doi:10.24875/ric.17002064 · Cited by 9
Categorical predictive and disease progression modeling in the early stage of Alzheimer’s disease
Platero, C. A. (2022) · Journal of Neuroscience Methods · doi:10.1016/j.jneumeth.2022.109581 · Cited by 8
“Several groups have attempted to characterize this subtle cognitive impairment using a single cutoff point on a global cognitive domain score (Jack et al., 2012), or with a memory composite score (Vos et al., 2013) or with subtle decline in functional abilities (Edmonds et al., 2015).”
Vilca, B. N. C., Rodríguez‐Rojo, I. C., Torres-Simón, L., Cuesta, P., Carnes, A., Piñol‐Ripoll, G., Huerto, R. P., Tahan, N., & Maestú, F. (2022) · Clinical Neurophysiology · doi:10.1016/j.clinph.2022.08.007 · Cited by 10
Using the A/T/N Framework to Examine Driving in Preclinical Alzheimer’s Disease
Roe, C. M., Babulal, G. M., Stout, S. H., Carr, D. B., Williams, M., Benzinger, T. L. S., Fagan, A. M., Holtzman, D. M., Ances, B. M., & Morris, J. C. (2018) · Geriatrics · doi:10.3390/geriatrics3020023 · Cited by 9
““T+” was assigned when CSF ptau181 ≥ 67 pg/mL and “N+” when tau ≥ 339 pg/mL [15].”
Self-citationDifferences in Driving Outcomes Among Cognitively Normal African American and Caucasian Older Adults
Babulal, G. M., Stout, S. H., Williams, M. M., Rajasekar, G., Harmon, A. C., Vivoda, J. M., Zuelsdorff, M. L., Benzinger, T. L. S., Morris, J. C., Ances, B. M., et al. (2019) · Journal of Racial and Ethnic Health Disparities · doi:10.1007/s40615-019-00655-z · Cited by 9
Self-citationNew Frontiers for Collaborative Research
Goldman, M. (2013) · Science Translational Medicine · doi:10.1126/scitranslmed.3007990 · Cited by 9
Blake, M., Brown, D. C., Chen, C., Al-Hammadi, N. J., Casanova, R., Zhu, Y., & Babulal, G. M. (2025) · Scientific Data · doi:10.1038/s41597-025-05554-z · Cited by 10
“Preclinical AD is the asymptomatic stage (~15–20 years) where the pathophysiology onset has catalyzed without symptoms of cognitive impairment 8 .”
Deng, Z., Xie, D., Cai, J., Jiang, J., Pan, D., Liao, H., Liu, X., Xu, Y., Li, H., Shen, Q., et al. (2023) · Clinical Nutrition · doi:10.1016/j.clnu.2023.08.019 · Cited by 8
Hu, H., Hu, H., Jiang, J., Bi, Y., Sun, Y. P., Ou, Y., Tan, L., & Yu, J. (2024) · Alzheimer s & Dementia · doi:10.1002/alz.13837 · Cited by 8
Types and sources of medical and other related data
Pezoulas, V. C., Exarchos, T. P., & Fotiadis, D. I. (2020) · Elsevier eBooks · doi:10.1016/b978-0-12-816507-2.00002-5 · Cited by 8
A new era for dementia epidemiology: Alzheimer’s disease, hardening of arteries, or just old age?
Kuller, L. H. (2018) · European Journal of Epidemiology · doi:10.1007/s10654-018-0420-x · Cited by 8
Hessen, E., Kirsebom, B., Eriksson, C. M., Eliassen, C. F., Nakling, A. E., Bråthen, G., Waterloo, K. K., Aarsland, D., & Fladby, T. (2018) · Journal of Alzheimer s Disease · doi:10.3233/jad-180964 · Cited by 7
“A similar finding was reported in a five-year follow up [10] where a progression rate to probable mild dementia (CDR ≥0.”
BackgroundResult
Metadata
- Authors
- Vos, S. J., Xiong, C., Visser, P. J., Jasielec, M. S., Hassenstab, J., Grant, E. A., Cairns, N. J., Morris, J. C., Holtzman, D. M., & Fagan, A. M.
- Affiliations
- Maastricht University (NL)
- Washington University in St. Louis (US)
- Corresponding author
- Vos, Stephanie JB
- Fagan, Anne M
- ORCID
- Venue
- The Lancet Neurology
- Publisher
- Elsevier BV
- Published
- 2013-10
- Volume
- 12
- Issue
- 10
- Pages
- 957-965
- ISSN
- 1474-4422 (ISSN-L)
- PMC
- PMC3904678
- OpenAlex
- W2096063777
- Cited by
- 564
- References
- 45
- Citations by year
- 2026: 20 · 2025: 37 · 2024: 30 · 2023: 17 · 2022: 40 · 2021: 39 · 2020: 45 · 2019: 54 · 2018: 63 · 2017: 54 · 2016: 53 · 2015: 52 · 2014: 52 · 2013: 7
- FWCI
- 38.74
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The Lancet Neurology (publishedVersion)
- PubMed (publishedVersion)
- Research Publications (Maastricht University) (publishedVersion)
- Pure Amsterdam UMC (publishedVersion)
- Amsterdam UMC (VU Amsterdam) - Institutional Repository (publishedVersion)
- PubMed Central (acceptedVersion)
- Research Publications (Maastricht University) (submittedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Funders
- Mayo Clinic
- Center for Translational Molecular Medicine
- National Institute on Aging (P 50 AG05681, P50AG005681, P01AG003991, U19AG032438, P01-AG02676, P01AG026276)
- National Institute of Diabetes and Digestive and Kidney Diseases (K23DK094982)
- National Institute of Neurological Disorders and Stroke (P30NS057105)
- 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 › Oncology › Cancer-related cognitive impairment studies
- Keywords
- preclinical Alzheimer's disease, amyloid-beta 42, tau protein, cerebrospinal fluid biomarkers, cognitive decline, conversion to dementia, mortality, prevalence, cognitively normal elderly, Alzheimer's disease staging, community-dwelling older adults
- MeSH terms
- Aged, Aged, 80 and over, Alzheimer Disease, Apolipoproteins E, Brain, Female, Humans, Longitudinal Studies, Male, Middle Aged, Neuropsychological Tests, Peptide Fragments, Psychiatric Status Rating Scales, Severity of Illness Index, Prevalence, Survival Analysis, Amyloid beta-Peptides, tau Proteins, Disease Progression, Memory, Episodic, Prodromal Symptoms
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