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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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“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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“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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“decline and mortality (Vos et al., 2013); however, several neuro-”
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Jack, C. R., Wiste, H. J., Weigand, S. D., Knopman, D. S., Mielke, M. M., Vemuri, P., Lowe, V. J., Senjem, M. L., Gunter, J. L., Reyes, D. A., et al. (2015) · Brain · doi:10.1093/brain/awv283 · Cited by 258
“Others have also found amyloid-b independent Alzheimer’s disease-like neurodegenerative biomarker abnormalities in cognitively normal (Jack et al., 2013b; van Harten et al., 2013; Vos et al., 2013; Wirth et al., 2013a, 2013b; Mormino et al., 2014b; Toledo et al., 2014) and mildly impaired subjects (Duara et al.”
BackgroundDubois, B., Epelbaum, S., Nyasse, F., Bakardjian, H., Gagliardi, G. P., Uspenskaya, O., Houot, M., Lista, S., Cacciamani, F., Potier, M., et al. (2018) · The Lancet Neurology · doi:10.1016/s1474-4422(18)30029-2 · Cited by 253
EEG evidence of compensatory mechanisms in preclinical Alzheimer’s disease
Gaubert, S., Raimondo, F., Houot, M., Corsi, M., Naccache, L., Sitt, J. D., Hermann, B., Oudiette, D., Gagliardi, G. P., Habert, M., et al. (2019) · Brain · doi:10.1093/brain/awz150 · Cited by 243
“Moreover, very few studies of early stages of Alzheimer’s disease consider neurodegeneration information when selecting subjects, whereas it has been suggested that studies combining an abnormal amyloid biomarker with an abnormal neurodegeneration biomarker provide much more powerful prediction of future cognitive dec…”
Roberts, R. O., Aakre, J. A., Kremers, W. K., Vassilaki, M., Knopman, D. S., Mielke, M. M., Alhurani, R., Geda, Y. E., Machulda, M. M., Coloma, P., et al. (2018) · JAMA Neurology · doi:10.1001/jamaneurol.2018.0629 · Cited by 223
Hata, M., Kazui, H., Tanaka, T., Ishii, R., Canuet, L., Pascual-Marqui, R. D., Aoki, Y., Ikeda, S., Kanemoto, H., Yoshiyama, K., et al. (2015) · Clinical Neurophysiology · doi:10.1016/j.clinph.2015.10.030 · Cited by 235
“The global CDR scores are 0, meaning cognitive normality, 0.5, 1, 2, and 3, meaning very mild cognitive impairment, and mild, moderate, severe dementia, respectively (Vos et al., 2013).”
InfluentialBarthélemy, N. R., Bateman, R. J., Hirtz, C., Marin, P., Becher, F., Sato, C., Gabelle, A., & Lehmann, S. (2020) · Alzheimer's Research & Therapy · doi:10.1186/s13195-020-00596-4 · Cited by 229
Mild Cognitive Impairment: the Manchester consensus
Dunne, R. A., Aarsland, D., O'Brien, J. T., Ballard, C. G., Banerjee, S., Fox, N. C., Isaacs, J. D., Underwood, B. R., Perry, R. J., Chan, D., et al. (2020) · Age and Ageing · doi:10.1093/ageing/afaa228 · Cited by 240
Magnetic resonance imaging in Alzheimer’s disease neuroimaging initiative 2
Jack, C. R., Barnes, J., Bernstein, M. A., Borowski, B. J., Brewer, J., Clegg, S., Dale, A. M., Carmichael, O., Ching, C., DeCarli, C., et al. (2015) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2015.05.002 · Cited by 220
“[126] Vos SJ, Xiong C, Visser PJ, Jasielec MS, Hassenstab J, Grant EA, et al.”
BackgroundBurnham, S. C., Bourgeat, P., Doré, V., Savage, G., Brown, B., Laws, S., Maruff, P., Salvado, O., Ames, D., Martins, R. N., et al. (2016) · The Lancet Neurology · doi:10.1016/s1474-4422(16)30125-9 · Cited by 207
El-Hayek, Y. H., Wiley, R. E., Khoury, C. P., Daya, R. P., Ballard, C., Evans, A. R., Karran, M., Molinuevo, J. L., Norton, M., & Atri, A. (2019) · Journal of Alzheimer's Disease · doi:10.3233/jad-190426 · Cited by 216
“Addi720 tionally, patients with MCI also contend with an 721 increased risk of mortality [106].”
BackgroundSpatial Navigation in Preclinical Alzheimer’s Disease
Allison, S. L., Fagan, A. M., Morris, J. C., & Head, D. M. (2016) · Journal of Alzheimer s Disease · doi:10.3233/jad-150855 · Cited by 237
“In addition, CN individuals with amyloid deposition demonstrate greater atrophy as well as an increased risk of cognitive decline and development of symptomatic AD [18–22].”
Self-citationATN classification and clinical progression in subjective cognitive decline: The SCIENCe project
Ebenau, J. L., Timmers, T., Wesselman, L. M. P., Verberk, I. M. W., Verfaillie, S. C. J., Slot, R. E. R., van Harten, A. C., Teunissen, C. E., Barkhof, F., van den Bosch, K. A., et al. (2020) · Neurology · doi:10.1212/wnl.0000000000009724 · Cited by 191
Self-citationAmyloid-β and Tau at the Crossroads of Alzheimer’s Disease
Gallardo, G., & Holtzman, D. M. (2019) · Advances in experimental medicine and biology · doi:10.1007/978-981-32-9358-8_16 · Cited by 212
Self-citationCauses and Patterns of Dementia: An Update in the Era of Redefining Alzheimer's Disease
James, B. D., & Bennett, D. A. (2019) · Annual Review of Public Health · doi:10.1146/annurev-publhealth-040218-043758 · Cited by 213
Subtle Cognitive Decline and Biomarker Staging in Preclinical Alzheimer’s Disease
Edmonds, E. C., Initiative, A. D. N., Delano‐Wood, L., Galasko, D. R., Salmon, D. P., & Bondi, M. W. (2015) · Journal of Alzheimer s Disease · doi:10.3233/jad-150128 · Cited by 205
“This group has been referred to by Jack and others [9, 34, 35] as “suspected non-AD pathophysiology” (SNAP).”
BackgroundCentiloid cut-off values for optimal agreement between PET and CSF core AD biomarkers
for the Alzheimer’s Disease Neuroimaging Initiative, F. T. A. S., Salvadó, G., Molinuevo, J. L., Brugulat-Serrat, A., Falcon, C., Grau-Rivera, O., Suárez-Calvet, M., Pavia, J., Niñerola-Baizán, A., Perissinotti, A., et al. (2019) · Alzheimer's Research & Therapy · doi:10.1186/s13195-019-0478-z · Cited by 195
“hallmark of Alzheimer disease (AD) and occurs decades before the onset of clinical symptoms occur [1, 2].”
BackgroundParnetti, L., Chipi, E., Salvadori, N., D’Andrea, K., & Eusebi, P. (2019) · Alzheimer s Research & Therapy · doi:10.1186/s13195-018-0459-7 · Cited by 206
“…addressed Van Harten et al., 2013 [95] Amsterdam Dementia Cohort SMC 132 MCI–dementiab 1.5 3% (2/80) 18% (2/11) 60% (6/10) Not specifically addressed Vos et al., 2013 [62] WU-ADRC CN 311 MCIc 3.4 2% (2/129) 13% (6/47) 25% (9/36) 54% (7/13) AD Alzheimer’s disease, ADNI Alzheimer’s Disease…”
InfluentialCerebrospinal fluid p-tau231 as an early indicator of emerging pathology in Alzheimer's disease
Ashton, N. J., Benedet, A. L., Pascoal, T. A., Karikari, T. K., Lantero-Rodriguez, J., Brum, W. S., Mathotaarachchi, S., Therriault, J., Savard, M., Chamoun, M., et al. (2022) · eBioMedicine · doi:10.1016/j.ebiom.2022.103836 · Cited by 184
Molinuevo, J. L., Gramunt, N., Gispert, J. D., Fauria, K., Esteller, M., Minguillón, C., Sánchez‐Benavides, G., Huesa, G., Morán, S., Dal‐Ré, R., et al. (2016) · Alzheimer s & Dementia Translational Research & Clinical Interventions · doi:10.1016/j.trci.2016.02.003 · Cited by 181
“studies show that AD pathology develops for several years or even decades before clinical symptoms appear; this silent asymptomatic period of the disease is referred to as the preclinical stage of AD [11].”
BackgroundThe State of The Art on Acetylcholinesterase Inhibitors in the Treatment of Alzheimer’s Disease
Vecchio, I., Sorrentino, L., Paoletti, A., Marra, R., & Arbitrio, M. (2021) · Journal of Central Nervous System Disease · doi:10.1177/11795735211029113 · Cited by 189
PART, a distinct tauopathy, different from classical sporadic Alzheimer disease.
Jellinger, K. A., Alafuzoff, I., Attems, J., Beach, T. G., Cairns, N. J., Crary, J. F., Dickson, D. W., Hof, P. R., Hyman, B. T., Jack, C. R., et al. (2015) · Acta Neuropathologica · doi:10.1007/s00401-015-1407-2 · Cited by 171
“At this point in the introduction of molecular imaging for tau (tau PET), SNAP has not been addressed; however, there are CSF studies on both Aβ and tau that have come to largely the same conclusions of the imaging biomarker studies [44, 52–54].”
ResultSelf-citationIt's complicated: The relationship between sleep and Alzheimer's disease in humans
Lucey, B. P. (2020) · Neurobiology of Disease · doi:10.1016/j.nbd.2020.105031 · Cited by 172
Detection and treatment of Alzheimer’s disease in its preclinical stage
Rafii, M. S., & Aisen, P. S. S. (2023) · Nature Aging · doi:10.1038/s43587-023-00410-4 · Cited by 179
Amyloid precursor protein metabolism and inflammation markers in preclinical Alzheimer disease
Alcolea, D., Martínez-Lage, P., Sánchez-Juan, P., Olazarán, J., Antúnez, C., Izagirre, A., Ecay-Torres, M., Estanga, A., Clerigué, M., Guisasola, M. C., et al. (2015) · Neurology · doi:10.1212/wnl.0000000000001859 · Cited by 163
“11 For the analysis, stages 2 and 3 were combined due to the low number of participants in each group.”
Upadhaya, A. R., Kosterin, I., Kumar, S., Arnim, C. A. F. V., Yamaguchi, H., Fändrich, M., Walter, J., & Thal, D. R. (2014) · Brain · doi:10.1093/brain/awt362 · Cited by 170
“Therefore, the pathologically preclinical Alzheimer’s disease cases in our study cannot be compared with clinically detectable preclin- ical Alzheimer’s disease cases according to Vos et al. (2013).”
InfluentialCerebrospinal fluid biomarkers in trials for Alzheimer and Parkinson diseases
Lleó, A., Cavedo, E., Parnetti, L., Vanderstichele, H., Herukka, S., Andreasen, N., Ghidoni, R., Lewczuk, P., Jeromin, A., Winblad, B. G., et al. (2014) · Nature Reviews Neurology · doi:10.1038/nrneurol.2014.232 · Cited by 162
Self-citation“New Old Pathologies”: AD, PART, and Cerebral Age-Related TDP-43 With Sclerosis (CARTS)
Nelson, P. T., Trojanowski, J. Q., Abner, E. L., Al-Janabi, O. M., Jicha, G. A., Schmitt, F. A., Smith, C. D., Fardo, D. W., Wang, W.-X., Kryscio, R. J., et al. (2016) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlw033 · Cited by 158
Fasae, K. D., Abolaji, A. O., Faloye, T. R., Odunsi, A., Oyetayo, B. O., Enya, J. I., Rotimi, J. A., Akinyemi, R., Whitworth, A. J., & Aschner, M. (2021) · Journal of Trace Elements in Medicine and Biology · doi:10.1016/j.jtemb.2021.126779 · Cited by 161
de Wilde, A., van der Flier, W. M., Pelkmans, W., Bouwman, F. H., Verwer, J. H., Groot, C., van Buchem, M. M., Zwan, M. D., Ossenkoppele, R., Yaqub, M. M., et al. (2018) · JAMA Neurology · doi:10.1001/jamaneurol.2018.1346 · Cited by 154
Crous-Bou, M., Gascon, M., Gispert, J. D., Cirach, M., Sánchez-Benavides, G., Falcon, C., Arenaza-Urquijo, E. M., Gotsens, X., Fauria, K., Sunyer, J., et al. (2020) · Environment International · doi:10.1016/j.envint.2020.105546 · Cited by 145
Rabinovici, G. D., Knopman, D. S., Arbizu, J., Benzinger, T. L. S., Donohoe, K. J., Hansson, O., Herscovitch, P., Kuo, P. H., Lingler, J. H., Minoshima, S., et al. (2025) · Alzheimer s & Dementia · doi:10.1002/alz.14338 · Cited by 163
Alzheimer disease in African American individuals: increased incidence or not enough data?
Barnes, L. L. (2022) · Nature Reviews Neurology · doi:10.1038/s41582-021-00589-3 · Cited by 142
Kester, M. I., Teunissen, C. E., Sutphen, C., Herries, E. M., Ladenson, J. H., Xiong, C., Scheltens, P., van der Flier, W. M., Morris, J. C., Holtzman, D. M., et al. (2015) · Alzheimer's Research & Therapy · doi:10.1186/s13195-015-0142-1 · Cited by 146
“In addition, these “classical CSF biomarkers” predict progression to AD in cognitively normal individuals and individuals with mild cognitive impairment (MCI) [16, 18, 23, 47].”
BackgroundSelf-citationZhang, Y. S., Zhou, N., Knoll, B., Samra, S., Ward, M., Weıntraub, S., & Fawzi, A. A. (2019) · PLoS ONE · doi:10.1371/journal.pone.0214685 · Cited by 146
Fortea, J., Vilaplana, E., Alcolea, D. A., Carmona‐Iragui, M., Sánchez‐Saudinós, M., Sala, I., Antón‐Aguirre, S., González‐Ortiz, S., Medrano, S., Pegueroles, J., et al. (2014) · Annals of Neurology · doi:10.1002/ana.24186 · Cited by 140
“This finding is in agreement with Vos and colleagues’ work, in which the progression rate of participants in the SNAP group (CSF tau was used as a marker of neuronal injury) did not differ from that of individuals classed as normal as opposed to stages 2 and 3, in which higher progression rates were found.(35) Third,…”
ResultMild cognitive impairment with suspected nonamyloid pathology (SNAP): Prediction of progression
Caroli, A., Prestia, A., Galluzzi, S., Ferrari, C., van der Flier, W. M., Ossenkoppele, R., Van Berckel, B., Barkhof, F., Teunissen, C., Wall, A. E., et al. (2015) · Neurology · doi:10.1212/wnl.0000000000001209 · Cited by 142
“However, our findings are in contrast to previous studies that found a relative cognitive stability of cognitively normal elders with SNAP and showed that their cognitive progression was markedly lower than in amyloid-positive persons.(19,20) Such discrepancy suggests that patients with MCI-SNAP may represent a differ…”
ResultSelf-citationMood Changes in Cognitively Normal Older Adults are Linked to Alzheimer Disease Biomarker Levels
Babulal, G. M., Ghoshal, N., Head, D. M., Vernon, E. K., Holtzman, D. M., Benzinger, T. L. S., Fagan, A. M., Morris, J. C., & Roe, C. M. (2016) · American Journal of Geriatric Psychiatry · doi:10.1016/j.jagp.2016.04.004 · Cited by 149
Self-citationBlood-Based Biomarkers for Alzheimer’s Disease Diagnosis and Progression: An Overview
Varesi, A., Carrara, A., Pires, V. G., Floris, V., Pierella, E., Savioli, G., Prasad, S., Esposito, C., Ricevuti, G., Chirumbolo, S., et al. (2022) · Cells · doi:10.3390/cells11081367 · Cited by 150
“This is not surprising considering that CSF Aβ peptides represent one of the core biomarkers in AD diagnosis, and that, at the same time, there is an urgent need to identify more accessible ones [37,38].”
BackgroundAbsence of practice effects in preclinical Alzheimer’s disease.
Hassenstab, J. J., Ruvolo, D., Jasielec, M. S., Xiong, C., Grant, E., & Morris, J. C. (2015) · Neuropsychology · doi:10.1037/neu0000208 · Cited by 145
“…of clinically evident cognitive deficits is marked by “subtle cognitive decline,” and although these subtle changes have been variously operationalized, support is now emerging that their presence is highly predictive of progression to symptomatic AD (Knopman et al., 2012; Vos et al., 2013).”
BackgroundInfluentialSelf-citationAssociation of Cerebral Amyloid-β Aggregation With Cognitive Functioning in Persons Without Dementia
Jansen, W. J., Ossenkoppele, R., Tijms, B. M., Fagan, A. M., Hansson, O., Klunk, W. E., van der Flier, W. M., Villemagne, V. L., Frisoni, G. B., Fleisher, A., et al. (2017) · JAMA Psychiatry · doi:10.1001/jamapsychiatry.2017.3391 · Cited by 147
Self-citationObjective subtle cognitive difficulties predict future amyloid accumulation and neurodegeneration
Thomas, K. R., Bangen, K. J., Weigand, A. J., Edmonds, E. C., Wong, C. G., Cooper, S., Delano‐Wood, L., Bondi, M. W., & Initiative, A. D. N. (2019) · Neurology · doi:10.1212/wnl.0000000000008838 · Cited by 144
Tau: From research to clinical development
Holtzman, D. M., Carrillo, M. C., Hendrix, J. A., Bain, L. J., Catafau, A. M., Gault, L. M., Goedert, M., Mandelkow, E., Mandelkow, E., Miller, D. S., et al. (2016) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2016.03.018 · Cited by 139
“Reflecting the fact that increases in CSF tau somehow reflect the process of neurodegeneration in AD, it has been shown that cognitively normal people with high levels of tau combined with low Ab42 almost all progressed to mild dementia or mild cognitive impairment (MCI) [31]; and those with MCI progressed to AD [32].”
Self-citationDetermining clinically meaningful decline in preclinical Alzheimer disease
Insel, P. S., Weiner, M., Mackin, R. S., Mormino, E., Lim, Y. Y., Stomrud, E., Palmqvist, S., Masters, C. L., Maruff, P. T., Hansson, O., et al. (2019) · Neurology · doi:10.1212/wnl.0000000000007831 · Cited by 128
Nerve growth factor metabolic dysfunction in Alzheimer's disease and Down syndrome
Iulita, M. F., & Cuello, A. C. (2014) · Trends in Pharmacological Sciences · doi:10.1016/j.tips.2014.04.010 · Cited by 141
Initiative, A. D. N., Pascoal, T. A., Mathotaarachchi, S. S., Mohades, S. T., Benedet, A. L., Chung, C.-O., Shin, M., Wang, S., Beaudry, T., Kang, M. S., et al. (2016) · Molecular Psychiatry · doi:10.1038/mp.2016.37 · Cited by 137
Subthreshold Amyloid Predicts Tau Deposition in Aging
Leal, S. L., Lockhart, S. N., Maaß, A., Bell, R. K., & Jagust, W. J. (2018) · Journal of Neuroscience · doi:10.1523/jneurosci.0485-18.2018 · Cited by 137
“, 2011b), are likely to be at risk for the development of AD (Vos et al., 2013; Donohue et al., 2017), and are thus potential targets of pharmacologic intervention before showing symptoms (Sperling et al.”
BackgroundButterfield, D. A. (2014) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2014.06.006 · Cited by 126
“AD (PCAD) is gaining acceptance as the earliest form of AD [14].”
BackgroundUddin, M. S., Kabir, M. T., Rahman, M. S., Behl, T., Jeandet, P., Ashraf, G. M., Najda, A., Bin-Jumah, M. N., El-Seedi, H. R., & Abdel‐Daim, M. M. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21165858 · Cited by 131
Lim, Y. Y., Villemagne, V. L., Laws, S. M., Pietrzak, R. H., Snyder, P. J., Ames, D. J., Ellis, K. A., Harrington, K., Rembach, A., Martins, R. N., et al. (2014) · Molecular Psychiatry · doi:10.1038/mp.2014.123 · Cited by 126
Hansson, O., Mikulskis, A., Fagan, A. M., Teunissen, C. E., Zetterberg, H., Vanderstichele, H., Molinuevo, J. L., Shaw, L. M. J., Vandijck, M. L. J., Verbeek, M. M., et al. (2018) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2018.05.008 · Cited by 123
“Promisingly, these biomarkers also detect pathological changes associated with preclinical AD in cognitively healthy elderly individuals [14,54,60,61] and can enhance both differential diagnosis and prognostic stratification within AD populations.”
BackgroundSelf-citationPrevalence of preclinical Alzheimer disease
Kern, S., Zetterberg, H., Kern, J., Zettergren, A., Wærn, M., Höglund, K., Andréasson, U., Wetterberg, H., Börjesson‐Hanson, A., Blennow, K., et al. (2018) · Neurology · doi:10.1212/wnl.0000000000005476 · Cited by 123
“In accordance with the criteria from Dubois et al.,17 persons with both amyloid and tau pathology were classified as having preclinical AD.”
BackgroundResultInfluential
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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