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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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“Using tertile cut points, the proportion of individuals classified into the 2011 NIA-AA/SNAP stages was comparable to prior studies that used clinically validated cut points.(5,7,12) In followup sensitivity analyses, other cut points were used, including (1) quartiles for all biomarkers or (2) tertiles for Aβ1–42 and…”
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“Although recent data support many aspects of this model [2,16,26,56–58], some do not and the model has been updated accordingly [34].”
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“necessarily imply that clinical ADwill result but does appear to come with a higher risk of developing clinical AD [4].”
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“Two of the four autopsy reports [41] described medial temporal tauopathy without amyloidosis—i.”
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“Moreover, CSF t-tau is abnormally increased in 50% of preclinical AD individuals, when neurodegeneration is limited [5].”
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“5 We corroborate findings from multiple reports showing that among initially CN older adults, abnormal A 𝛽 is associated with both cognitive decline 7,9 and functional progression.”
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“The presence of one CSF biomarker of AD, either CSF A or CSF tau/ptau, is interpretedas a biomarker of intermediate likelihood [7].”
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“It is worth noting that the slow progression in this SNAP-MCI group is akin to prior studies of cognitively normal SNAP patients (Knopman et al., 2012; Vos et al., 2013).”
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“…large public health burden and the fact that techniques now exist to diagnose neurodegenerative disorders such as Alzheimer disease before clinical symptoms develop, 44,45 is to determine whether sleep deficiency/sleep disorders represent modifiable risk factors that can alter disease progression.”
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“Current recommendations to ameliorate risk of cognitive decline due to AD or other causes involve optimizing treatment of vascular risk factors, in addition to lifestyle factors that highlight the importance of physical, cognitive, and social activity; diet; and adequate sleep.”
Schindler, S. E., Jasielec, M. S., Weng, H., Hassenstab, J. J., Grober, E. H., McCue, L. M., Morris, J. C., Holtzman, D. M., Xiong, C., & Fagan, A. M. (2017) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2017.04.004 · Cited by 77
Self-citationPreclinical Alzheimer's disease: A systematic review of the cohorts underlying the concept
Epelbaum, S., Genthon, R., Cavedo, E., Habert, M. O., Lamari, F., Gagliardi, G. P., Lista, S., Teichmann, M., Bakardjian, H., Hampel, H. J., et al. (2017) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2016.12.003 · Cited by 82
“…Postmortem neuropathologic evaluations Snowdon et al. (1996) [69] Yes Yes Yes No Optional Yes None Alcolea et al. (2015) [70] Yes Yes No No No Yes No Vos et al. (2013) [71] Yes No No No No Yes No Sager et al. (2005) [72]; La Rue et al. (2008) [73] Initiative, the Australian Imaging, the…”
BackgroundInsel, P. S., Ossenkoppele, R., Gessert, D., Jagust, W., Landau, S. M., Hansson, O., Weiner, M. W., & Mattsson, N. (2017) · Frontiers in Neuroscience · doi:10.3389/fnins.2017.00281 · Cited by 75
“This is in accordance with previous reports showing that preclinical AD may persist for several years before development of significant cognitive impairment, i.e., prodromal AD (Vos et al., 2013; Jansen et al., 2015).”
ResultHampel, H. J., Schneider, L. S., Giacobini, E., Kivipelto, M., Sindi, S., Dubois, B., Broich, K., Nisticò, R., Aisen, P. S. S., & Lista, S. (2014) · Expert Review of Neurotherapeutics · doi:10.1586/14737175.2015.995637 · Cited by 82
“Until now, the risk of conversion to a clinical AD has been established around 25% after 3 years [154] or after 5 years of follow-up for subjects who are at stage 2, that is, subjects with evidence of both amyloid and neuronal injury markers [155].”
BackgroundAnti-amyloid-β protein agents for the treatment of Alzheimer’s disease: an update on emerging drugs
Lozupone, M., Solfrizzi, V., D’Urso, F., Di Gioia, I., Sardone, R., Dibello, V., Stallone, R., Liguori, A., Ciritella, C., Daniele, A., et al. (2020) · Expert Opinion on Emerging Drugs · doi:10.1080/14728214.2020.1808621 · Cited by 77
Li, Q., Villemagne, V. L., Doecke, J. D., Rembach, A., Sarros, S., Varghese, S., McGlade, A. R., Laughton, K. M., Pertile, K. K., Fowler, C. J., et al. (2015) · Journal of Alzheimer s Disease · doi:10.3233/jad-150247 · Cited by 75
“Our findings support both scenarios, with perhaps ∼30% of the MCI/AD group misdiagnosed based on the combination of CSF and PET imaging results and aligned to previous studies that have found 30% of cognitively normal subjects over 60 years of age display abnormal AD biomarkers [7, 8, 26, 40] or plaques [26–28].”
ResultThe EMIF-AD PreclinAD study: study design and baseline cohort overview
Konijnenberg, E., Carter, S. F., ten Kate, M., den Braber, A., Tomassen, J., Amadi, C., Wesselman, L. M. P., Nguyen, H., van de Kreeke, J. A., Yaqub, M. M., et al. (2018) · Alzheimer s Research & Therapy · doi:10.1186/s13195-018-0406-7 · Cited by 77
“Third, amyloid pathology has been associated with an increased risk for cognitive decline, but the rate of decline varies greatly [19].”
BackgroundSelf-citationThe Importance of the Validation of M/EEG With Current Biomarkers in Alzheimer's Disease
Maestú, F., Cuesta, P., Hasan, O., Fernández, A., Funke, M. E., & Schulz, P. E. (2019) · Frontiers in Human Neuroscience · doi:10.3389/fnhum.2019.00017 · Cited by 78
“, 2001) and its deposits correlates with cognitive impairment (Nelson et al., 2012; Vos et al., 2013; Albert et al., 2018) and network dysfunction (Schultz et al.”
BackgroundSubjective cognitive decline: Memory complaints, cognitive awareness, and metacognition
Cappa, S. F., Ribaldi, F., Chicherio, C., & Frisoni, G. B. (2024) · Alzheimer s & Dementia · doi:10.1002/alz.13905 · Cited by 83
Microfinance literature: A sustainability level perspective survey
Pérez, I. G., Torres, M. J. M., & Izquierdo, M. Á. F. (2016) · Journal of Cleaner Production · doi:10.1016/j.jclepro.2016.10.128 · Cited by 80
Understanding the cause of sporadic Alzheimer’s disease
Zetterberg, H., & Mattsson, N. (2014) · Expert Review of Neurotherapeutics · doi:10.1586/14737175.2014.915740 · Cited by 73
“However, besides a plethora of experimental data in disease models, whose validity for sporadic AD in humans is sometimes difficult to assess, the relevance of the Ab cascade hypothesis for sporadic AD is supported by biomarker studies showing increased risk of future cognitive impairment in healthy elderly people wit…”
BackgroundYu, J., Li, J., Suckling, J., Feng, L., Pan, A., Wang, Y., Song, B., Zhu, S., Li, D., Wang, H.-F., et al. (2019) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2019.05.006 · Cited by 72
“In CN group, frequency of A/N scheme were also conducted in Knight Alzheimer’s Disease Research Center [18].”
Prasad, H., & Rao, R. (2015) · Journal of Biological Chemistry · doi:10.1074/jbc.m114.602219 · Cited by 76
“With an aging population, Alzheimer and related neurodegenerative disorders pose a similar challenge (20).”
BackgroundAmyloid, Vascular, and Resilience Pathways Associated with Cognitive Aging
Vemuri, P., Lesnick, T. G., Knopman, D. S., Przybelski, S. A., Reid, R. I., Mielke, M. M., Graff‐Radford, J., Lowe, V. J., Machulda, M. M., Petersen, R. C., et al. (2019) · Annals of Neurology · doi:10.1002/ana.25600 · Cited by 74
Neuropsychological changes in asymptomatic persons with Alzheimer disease neuropathology
Monsell, S. E., Mock, C., Hassenstab, J., Roe, C. M., Cairns, N. J., Morris, J. C., & Kukull, W. (2014) · Neurology · doi:10.1212/wnl.0000000000000650 · Cited by 71
“, people with both amyloid deposition and evidence of neurodegeneration on biomarkers, as well as subtle cognitive changes).(37) It should be noted that such neuropsychological changes occur after neuronal degeneration, rather than after amyloid deposits alone.”
BackgroundSelf-citationEmerging β-amyloid pathology and accelerated cortical atrophy
Mattsson, N., Insel, P. S., Nosheny, R., Tosun, D., Trojanowski, J. Q., Shaw, L. M., Jack, C. R., Donohue, M. C., & Weiner, M. W. (2014) · JAMA Neurology · doi:10.1001/jamaneurol.2014.446 · Cited by 71
Biomarkers of Alzheimer's disease and mild cognitive impairment: A current perspective
Lewczuk, P., Mroczko, B., Fagan, A. M., & Kornhuber, J. (2014) · Advances in Medical Sciences · doi:10.1016/j.advms.2014.11.002 · Cited by 73
“Furthermore, this stage, as defined by biomarkers, has been shown to predict future cognitive decline, and thus is considered to represent a truly ‘‘pre-clinical’’ stage [88].”
BackgroundSelf-citationDescriptive Epidemiology of Neurodegenerative Diseases: What Are the Critical Questions?
Logroscino, G., Urso, D., & Savica, R. (2022) · Neuroepidemiology · doi:10.1159/000525639 · Cited by 79
Zavecz, Z., Shah, V. D., Murillo, O. G., Vallat, R., Mander, B. A., Winer, J. R., Jagust, W. J., & Walker, M. P. (2023) · BMC Medicine · doi:10.1186/s12916-023-02811-z · Cited by 67
“Second, the early stages of the AD pathological cascade, such as Aβ pathology [10], allow for cognitive reserve to the greatest extent, indicated by a higher proportion of cognitively normal elderly adults with only Aβ pathology than with Aβ pathology and neurodegeneration [34, 35].”
Backgroundd’Abramo, C., D'adamio, L., & Giliberto, L. (2020) · Journal of Personalized Medicine · doi:10.3390/jpm10030116 · Cited by 71
Blackburn, D. J., Wakefield, S., Shanks, M. F., Harkness, K. A., Reuber, M., & Venneri, A. (2014) · British Medical Bulletin · doi:10.1093/bmb/ldu029 · Cited by 74
Wang, Q., Wang, Y., Liu, J., Sutphen, C. L., Cruchaga, C., Blazey, T., Gordon, B. A., Su, Y., Chen, C., Shimony, J. S., et al. (2019) · NeuroImage: Clinical · doi:10.1016/j.nicl.2019.101767 · Cited by 63
Self-citationCurrent and evolving treatment strategies for the Alzheimer disease continuum
Marasco, R. (2020) · The American Journal of Managed Care · doi:10.37765/ajmc.2020.88481 · Cited by 67
Imbimbo, B. P., Ippati, S., Watling, M., & Imbimbo, C. (2022) · Pharmacological Research · doi:10.1016/j.phrs.2022.106631 · Cited by 69
Li, F., Xie, X.-Y., Sui, X.-F., Wang, P., Chen, Z., & Zhang, J. (2020) · Neuroscience · doi:10.1016/j.neuroscience.2020.02.044 · Cited by 67
Mormino, E. C., Papp, K. V., Rentz, D. M., Schultz, A. P., LaPoint, M. R., Amariglio, R. E., Hanseeuw, B. J., Marshall, G. A., Hedden, T., Johnson, K. A., et al. (2016) · JAMA Neurology · doi:10.1001/jamaneurol.2016.2237 · Cited by 63
Novel Anti-Alzheimer’s Therapeutic Molecules Targeting Amyloid Precursor Protein Processing
Uddin, M. S., Kabir, M. T., Jeandet, P., Mathew, B., Ashraf, G. M., Perveen, A., Bin-Jumah, M. N., Mousa, S. A., & Abdel‐Daim, M. M. (2020) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2020/7039138 · Cited by 67
“Crenezumab is an anti-Aβ monoclonal antibody with a specific affinity towards all fibrillary, oligomeric, and pentameric amyloids [161].”
BackgroundZou, C., Shi, Y., Ohli, J., Schüller, U., Dorostkar, M. M., & Herms, J. W. (2016) · Acta Neuropathologica · doi:10.1007/s00401-015-1527-8 · Cited by 67
“Subjects in the preclinical stages are at risk for future cognitive decline [51].”
BackgroundEarly brain connectivity alterations and cognitive impairment in a rat model of Alzheimer’s disease
Muñoz‐Moreno, E., Tudela, R., López-Gil, X., & Sòria, G. (2018) · Alzheimer s Research & Therapy · doi:10.1186/s13195-018-0346-2 · Cited by 65
de Wilde, A., van Buchem, M. M., Otten, R. H. J., Bouwman, F. H., Stephens, A. W., Barkhof, F., Scheltens, P., & van der Flier, W. M. (2018) · Alzheimer s Research & Therapy · doi:10.1186/s13195-018-0398-3 · Cited by 65
Spatial navigation ability predicts progression of dementia symptomatology
Levine, T. F., Allison, S. L., Stojanovic, M., Fagan, A. M., Morris, J. C., & Head, D. M. (2020) · Alzheimer s & Dementia · doi:10.1002/alz.12031 · Cited by 62
Self-citationBertens, D., Knol, D. L., Scheltens, P., Visser, P. J., & Initiative, A. D. N. (2014) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2014.05.1754 · Cited by 70
“Ourobservation that subjects in the AD-asymptomatic stage had abnormal CSF tau is in line with previous studies [20,21].”
Self-citationGrober, E. H., Veroff, A. E., & Lipton, R. B. (2018) · Alzheimer s & Dementia Diagnosis Assessment & Disease Monitoring · doi:10.1016/j.dadm.2017.12.004 · Cited by 68
Widespread distribution of tauopathy in preclinical Alzheimer's disease
Schultz, S. A., Gordon, B. A., Mishra, S., Su, Y., Perrin, R. J., Cairns, N. J., Morris, J. C., Ances, B. M., & Benzinger, T. L. S. (2018) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2018.08.022 · Cited by 65
“Multiple clinicopathologic studies demonstrate that AD pathology is present in individuals before clinical symptoms develop; such individuals are at elevated risk for progression to AD dementia (Fagan et al., 2007; Morris et al., 2009; Vos et al., 2013).”
BackgroundSelf-citationDeng, Z., Jiang, J., Wang, J., Pan, D., Zhu, Y., Li, H., Zhang, X., Liu, X., Xu, Y., Li, Y., et al. (2022) · Hypertension · doi:10.1161/hypertensionaha.122.19378 · Cited by 65
Ding, N., Jiang, J. H., Xu, A., Tang, Y., & Li, Z. (2019) · Frontiers in Neuroscience · doi:10.3389/fnins.2019.00037 · Cited by 63
Preclinical Alzheimer's disease and longitudinal driving decline
Roe, C. M., Babulal, G. M., Head, D. M., Stout, S. H., Vernon, E. K., Ghoshal, N., Garland, B., Barco, P. P., Williams, M., Johnson, A., et al. (2016) · Alzheimer s & Dementia Translational Research & Clinical Interventions · doi:10.1016/j.trci.2016.11.006 · Cited by 63
“Thus, as with cognitive outcomes [9], the risk of developing driving problems appears to be greatest when the preclinical AD biomarker profile is characterized by both cerebral betaamyloidosis and markers of neural injury, such as elevated levels of CSF tau and ptau181, rather than cerebral betaamyloidosis levels alon…”
BackgroundSelf-citationSequence of Alzheimer disease biomarker changes in cognitively normal adults
Luo, J. R., Agboola, F., Grant, E., Masters, C. L., Albert, M., Johnson, S. C., McDade, E., Vöglein, J., Fagan, A. M., Benzinger, T. L. S., et al. (2020) · Neurology · doi:10.1212/wnl.0000000000010747 · Cited by 59
Self-citationRostamzadeh, A., Bohr, L., Wagner, M., Baethge, C., & Jessen, F. (2022) · Neurology · doi:10.1212/wnl.0000000000201072 · Cited by 61
Molinuevo, J. L., Camı́, J., Carné, X., Carrillo, M. C., Georges, J., Isaac, M., Khachaturian, Z. S., Kim, S. Y. H., Morris, J. C., Pasquier, F., et al. (2016) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2016.01.009 · Cited by 63
“The validity of these stages has been suggested by a retrospective study of asymptomatic individuals which demonstrated that the 5-year progression rate was 2% for participants classified as normal, 11% for those in stage 1, 26% for stage 2, and 56% for stage 3 [14].”
BackgroundSelf-citationSmailagic, N., Lafortune, L., Kelly, S., Hyde, C., & Brayne, C. (2018) · Journal of Alzheimer’s Disease · doi:10.3233/jad-171125 · Cited by 61
“Discriminating between patients who will and will not progress to dementia due to AD is critical in the context of care and future therapies [9].”
BackgroundAlzheimer’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
“According to long-term observational research, those with cognitively normal brains are prone to developing dementia and MCI [40, 41].”
BackgroundClark, L. R., Koscik, R. L., Nicholas, C. R. N., Okonkwo, O. C., Engelman, C. D., Bratzke, L. C., Hogan, K. J., Mueller, K. D., Bendlin, B. B., Carlsson, C. M., et al. (2016) · Archives of Clinical Neuropsychology · doi:10.1093/arclin/acw024 · Cited by 65
Hsu, D. C., Study, F. T. H. A. B., Mormino, E. C., Schultz, A. P., Amariglio, R. E., Donovan, N. J., Rentz, D. M., Johnson, K. A., Sperling, R. A., & Marshall, G. A. (2016) · Journal of Alzheimer s Disease · doi:10.3233/jad-150987 · Cited by 60
Secondary prevention of Alzheimer’s dementia: neuroimaging contributions
ten Kate, M., Ingala, S., Schwarz, A. J., Fox, N. C., Chételat, G., van Berckel, B. N. M., Ewers, M., Foley, C., Gispert, J. D., Hill, D., et al. (2018) · Alzheimer s Research & Therapy · doi:10.1186/s13195-018-0438-z · Cited by 65
Self-citationReijs, B. L. R., Vos, S. J. B., Soininen, H. S., Lötjönen, J. M. P., Koikkalainen, J. R., Pikkarainen, M., Hall, A., Vanninen, R. L., Liu, Y., Herukka, S., et al. (2017) · Journal of Alzheimer s Disease · doi:10.3233/jad-170039 · Cited by 60
“These AD biomarkers are abnormal up to 25 years before the onset of AD-type dementia, which makes them valuable for early detection of AD ([5–7].”
Self-citationMachulda, M. M., Hagen, C. E., Wiste, H. J., Mielke, M. M., Knopman, D. S., Roberts, R. O., Vemuri, P., Lowe, V. J., Jack, C. R., & Petersen, R. C. (2016) · The Clinical Neuropsychologist · doi:10.1080/13854046.2016.1241303 · Cited by 63
Big Data and Dementia: Charting the Route Ahead for Research, Ethics, and Policy
Ienca, M., Vayena, E., & Blasimme, A. (2018) · Frontiers in Medicine · doi:10.3389/fmed.2018.00013 · Cited by 65
“Further efforts are underway to establish other biomarkers—genetic, biological, and combinations thereof—in both CSF and plasma (2), as well as attempts to look at cognitive decline on longitudinally longer scales (9).”
BackgroundKunst, J., Mareček, R., Klobušiaková, P., Balážová, Z., Anderková, Ľ., Elfmarková, N., & Rektorová, I. (2018) · Brain Topography · doi:10.1007/s10548-018-0675-2 · Cited by 59
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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