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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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Characteristics of subjective cognitive decline associated with amyloid positivity
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Self-citationCertified normal: Alzheimer's disease biomarkers and normative estimates of cognitive functioning
Hassenstab, J. J., Chasse, R., Grabow, P., Benzinger, T. L. S., Fagan, A. M., Xiong, C., Jasielec, M. S., Grant, E., & Morris, J. C. (2016) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2016.03.014 · Cited by 58
“As the focus of this manuscript was on the impact of preclinical Alzheimer’s disease on normative cognitive data, individuals with evidence of neurodegeneration alone, often referred to as suspected non-AD pathology (SNAP; (Jack et al., 2012; Vos et al., 2013), were not included in the PCAD group.”
BackgroundMethodResultInfluentialSelf-citationAmyloid deposition and brain structure as long-term predictors of MCI, dementia, and mortality
López, O. L., Becker, J. T., Chang, Y., Klunk, W. E., Mathis, C. A., Price, J., Aizenstein, H. J., Snitz, B. E., Cohen, A. D., DeKosky, S. T., et al. (2018) · Neurology · doi:10.1212/wnl.0000000000005549 · Cited by 57
“For example, HIP volume(11) and WMLs(12,13) are predictors of mortality in individuals younger than 80 years, and those with CSF markers of Aβ deposition and neuronal injury had increased risk of death.(14) Thus, we examined the relationships between the biomarkers and clinical disease accounting for the competing ris…”
BackgroundResultBrown, C. A., Schmitt, F. A., Smith, C. D., & Gold, B. T. (2019) · NeuroImage · doi:10.1016/j.neuroimage.2019.03.073 · Cited by 61
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Time to Diagnosis in Young Onset Alzheimer’s Disease: A Population-Based Study from Central Norway
Kvello-Alme, M., Bråthen, G., White, L. R., & Sando, S. B. (2021) · Journal of Alzheimer s Disease · doi:10.3233/jad-210090 · Cited by 58
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“[11] implies an annual transition rate of 16% from all-cause MCI to AD, with rates higher in those with prodromal AD (27%) than in other forms (7%).”
BackgroundGanguli, M., Albanese, E., Seshadri, S. S., Bennett, D. A., Lyketsos, C. G., Kukull, W. A., Skoog, I. G., & Hendrie, H. C. (2018) · Alzheimer Disease & Associated Disorders · doi:10.1097/wad.0000000000000237 · Cited by 56
Comparison of plasma and CSF biomarkers in predicting cognitive decline
Aschenbrenner, A. J., Li, Y., Henson, R. L., Volluz, K., Hassenstab, J. J., Verghese, P. B., West, T., Meyer, M. R., Kirmess, K. M., Fagan, A. M., et al. (2022) · Annals of Clinical and Translational Neurology · doi:10.1002/acn3.51670 · Cited by 59
“Individuals with subtle evidence of cognitive change, even if clinically normal, are at high risk of developing dementia.(6,7) Unfortunately, lumbar punctures and brain imaging are burdensome and expensive, limiting their use, especially when serial assessments are required.”
BackgroundSelf-citationAn Algorithm for Preclinical Diagnosis of Alzheimer's Disease
Khan, T. K. (2018) · Frontiers in Neuroscience · doi:10.3389/fnins.2018.00275 · Cited by 56
“A longitudinal cohort study showed CSF AD biomarkers (Aβ42 and tau) and Aβ-PET can distinguish preclinical AD as high risk and low-risk categories (Vos et al., 2013).”
BackgroundA genetically modified minipig model for Alzheimer’s disease with SORL1 haploinsufficiency
Andersen, O. M., Bøgh, N., Landau, A. M., Pløen, G. G., Jensen, A. M. G., Monti, G., Ulhøi, B. P., Nyengaard, J. R., Jacobsen, K. R., Jørgensen, M. M., et al. (2022) · Cell Reports Medicine · doi:10.1016/j.xcrm.2022.100740 · Cited by 48
“The abnormal elevation of CSF tau observed in AD is no longer thought to be driven by tangle formation or neurodegeneration per se but, rather, is an early event that reflects accelerated active secretion and one that seems to coincide with amyloid secretion.(22,64,65) Our findings of increased levels of amyloid and t…”
ResultRethinking on the concept of biomarkers in preclinical Alzheimer’s disease
Berti, V., Polito, C., Lombardi, G., Ferrari, C., Sorbi, S., & Pupi, A. (2016) · Neurological Sciences · doi:10.1007/s10072-016-2477-1 · Cited by 54
Tau-directed approaches for the treatment of Alzheimer’s disease: focus on leuco-methylthioninium
Seripa, D., Solfrizzi, V., Imbimbo, B. P., Daniele, A., Santamato, A., Lozupone, M., Zuliani, G., Greco, A., Logroscino, G., & Panza, F. (2016) · Expert Review of Neurotherapeutics · doi:10.1586/14737175.2016.1140039 · Cited by 50
“These pathological events can be detected via CSF sampling or brain imaging before the onset of clinical symptoms [196,197].”
BackgroundMcDade, E. (2022) · CONTINUUM Lifelong Learning in Neurology · doi:10.1212/con.0000000000001131 · Cited by 56
Emerging biomarkers and screening for cognitive frailty
Ruan, Q., D’Onofrio, G., Sancarlo, D., Greco, A., Lozupone, M., Seripa, D., Panza, F., & Yu, Z. (2017) · Aging Clinical and Experimental Research · doi:10.1007/s40520-017-0741-8 · Cited by 53
“5), 2% for normal subjects, 11% for stage 1, 26% for stage 2, 56% for stage 3, and 5% for suspected non-AD pathophysiology [46].”
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“A recent study of Vos and colleagues demonstrated that subjects with preclinical AD had a higher risk for development of AD [18].”
BackgroundBabulal, G. M., Stout, S. H., Benzinger, T. L. S., Ott, B. R., Carr, D. B., Webb, M. M., Traub, C. M., Addison, A., Morris, J. C., Warren, D. K., et al. (2017) · Journal of Applied Gerontology · doi:10.1177/0733464817690679 · Cited by 48
“18 indicating preclinical AD (biomarker positive) that is present in ~30% of older adults aged 65 or older (Roe et al., 2013; Roe et al., 2008; Vos et al., 2013).”
BackgroundMethodInfluentialSelf-citationSuspected non-Alzheimer's pathology – Is it non-Alzheimer's or non-amyloid?
Dani, M., Brooks, D. J., & Edison, P. (2017) · Ageing Research Reviews · doi:10.1016/j.arr.2017.02.003 · Cited by 50
Abnormal Structural Brain Connectome in Individuals with Preclinical Alzheimer’s Disease
Pereira, J. B., van Westen, D., Stomrud, E., Strandberg, T. O., Volpe, G., Westman, E., & Hansson, O. (2017) · Cerebral Cortex · doi:10.1093/cercor/bhx236 · Cited by 48
“Indeed, there is increasing evidence showing that the pathological changes in AD begin well before clinical symptoms by several years to decades (Villemagne et al. 2013; Vos et al. 2013).”
Association of midlife vascular risk and AD biomarkers with subsequent cognitive decline
Pettigrew, C. A., Soldan, A., Wang, J., Wang, M., Arthur, K. C., Moghekar, A., Gottesman, R. F., & Albert, M. (2020) · Neurology · doi:10.1212/wnl.0000000000010946 · Cited by 52
“This is important given that cognitively normal individuals with biomarker evidence of both amyloid and tau pathology/neurodegeneration (sometimes referred to as hypothetical stage 2(32)) are at the greatest risk for cognitive decline compared to those with only 1 or no abnormal AD biomarkers.(6,34,35) Similar to a pr…”
ResultLong, J. M., Coble, D. W., Xiong, C., Schindler, S. E., Perrin, R. J., Gordon, B. A., Benzinger, T. L. S., Grant, E., Fagan, A. M., Harari, O., et al. (2022) · Brain · doi:10.1093/brain/awac250 · Cited by 49
Self-citationErickson, P., Simrén, J., Brum, W. S., Ennis, G. E., Kollmorgen, G., Suridjan, I., Langhough, R. E., Jonaitis, E. M., Hulle, C. A. V., Betthauser, T. J., et al. (2023) · JAMA Neurology · doi:10.1001/jamaneurol.2023.2338 · Cited by 48
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“Thus, cognitively normal individuals with significant amyloid and tau pathology (assessed either by measuring cerebrospinal fluid (CSF) levels or by positron emission tomography (PET) techniques) are at high risk for progression toAD [57–60].”
BackgroundDiagnostic value of cerebrospinal fluid Aβ ratios in preclinical Alzheimer’s disease
Adamczuk, K., Schaeverbeke, J. M., Vanderstichele, H., Lilja, J., Nelissen, N., Laere, K. V., Dupont, P. J., Hilven, K., Poesen, K., & Vandenberghe, R. R. (2015) · Alzheimer s Research & Therapy · doi:10.1186/s13195-015-0159-5 · Cited by 49
“Preclinical [1, 2], or asymptomatic [3], Alzheimer’s disease (AD) is characterized by the presence of AD-related pathophysiological processes in the absence of cognitive deficits.”
BackgroundAdamczuk, K., Schaeverbeke, J. M., Nelissen, N., Neyens, V., Vandenbulcke, M., Goffin, K. E., Lilja, J., Hilven, K., Dupont, P. J., Laere, K. V., et al. (2015) · European Journal of Nuclear Medicine and Molecular Imaging · doi:10.1007/s00259-015-3156-9 · Cited by 48
Assessment of amyloid β in pathologically confirmed frontotemporal dementia syndromes
Tan, R. H., Kril, J. J., Yang, Y., Tom, N., Hodges, J. R., Villemagne, V. L., Rowe, C. C., Leyton, C. E., Kwok, J. B. J., Ittner, L. M., et al. (2017) · Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring · doi:10.1016/j.dadm.2017.05.005 · Cited by 48
“With the use of in vivo markers of Ab deposition, it has been proposed that a diagnosis of preclinical AD can be made even in the absence of cognitive impairment [33,34].”
BackgroundMemory, executive, and multidomain subtle cognitive impairment
Toledo, J. B., Bjerke, M., Chen, K., Rozycki, M., Jack, C. R., Weiner, M. W., Arnold, S. E., Reiman, E. M., Davatzikos, C. A., Shaw, L. M. J., et al. (2015) · Neurology · doi:10.1212/wnl.0000000000001738 · Cited by 48
Self-citationGordon, B. A., Zacks, J. M., Blazey, T., Benzinger, T. L. S., Morris, J. C., Fagan, A. M., Holtzman, D. M., & Balota, D. A. (2015) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2015.01.019 · Cited by 49
Self-citationNeuropsychological Profiles and Trajectories in Preclinical Alzheimer’s Disease
Ho, J. K., Nation, D. A., & Initiative, A. D. N. (2018) · Journal of the International Neuropsychological Society · doi:10.1017/s135561771800022x · Cited by 52
“These results are partly supported by similar findings in other studies which demonstrate that the co-occurrence of Aβ pathology and neurodegeneration appear to accelerate decline in cognitively normal individuals (Vos et al., 2013).”
ResultParkinson disease and cognitive impairment
Davis, A. A., & Racette, B. A. (2016) · Neurology Clinical Practice · doi:10.1212/cpj.0000000000000285 · Cited by 45
“5 (very mild dementia) was between 11% and 26%.(9) Further work is needed to address the relative relationships of PD-specific pathology vs other age-related neuropathology on the development of dementia in patients with PD.”
BackgroundMultidomain intervention and/or omega‐3 in nondemented elderly subjects according to amyloid status
Delrieu, J., Payoux, P., Carrié, I., Cantet, C., Weiner, M. W., Vellas, B. J., & Andrieu, S. (2019) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2019.07.008 · Cited by 49
“This result is consistent with the data in the literature which indicate that nondemented subjects with negative amyloid biomarkers show very slight cognitive decline [18].”
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Luo, J. R., Agboola, F., Grant, E., Morris, J. C., Masters, C. L., Albert, M., Johnson, S. C., McDade, E., Fagan, A. M., Benzinger, T. L. S., et al. (2022) · Brain · doi:10.1093/brain/awac238 · Cited by 47
Self-citationLi, G., Millard, S. P., Peskind, E. R., Zhang, J., Yu, C., Leverenz, J. B., Mayer, C. L., Shofer, J., Raskind, M. A., Quinn, J. F., et al. (2014) · JAMA Neurology · doi:10.1001/jamaneurol.2014.445 · Cited by 45
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Stricker, N. H., Lundt, E. S., Albertson, S. M., Machulda, M. M., Pudumjee, S. B., Kremers, W. K., Jack, C. R., Knopman, D. S., Petersen, R. C., & Mielke, M. M. (2020) · Journal of Alzheimer s Disease · doi:10.3233/jad-200087 · Cited by 44
“Cross-sectional definitions have included a <10th percentile cut-off score on composite measures of memory [7] or global cognition [6].”
Stomrud, E., Minthon, L., Zetterberg, H., Blennow, K., & Hansson, O. (2015) · Alzheimer s & Dementia Diagnosis Assessment & Disease Monitoring · doi:10.1016/j.dadm.2015.09.002 · Cited by 43
“Several studies imply that CSF can identify cognitively healthy elderly individuals that are at increased risk of subsequent development of cognitive decline [9–14].”
BackgroundResultPredicting Progression to Mild Cognitive Impairment
Petersen, R. C., Lundt, E. S., Therneau, T. M., Weigand, S. D., Knopman, D. S., Mielke, M. M., Roberts, R. O., Lowe, V. J., Machulda, M. M., Kremers, W. K., et al. (2018) · Annals of Neurology · doi:10.1002/ana.25388 · Cited by 43
“When cognitively unimpaired (CU) individuals are categorized based on having normal (−) or abnormal (+) levels of A and N, the A+N+ group consistently has an elevated risk of progression to subsequent cognitive impairment.(6,7) Whether A−N+, also termed suspected non-Alzheimer pathophysiology (SNAP),(8) is a risk fact…”
BackgroundMethodDiagnostic biomarkers in Alzheimer’s disease
Andersen, E., Casteigne, B., Chapman, W. D., Creed, A., Foster, F., Lapins, A., Shatz, R., & Sawyer, R. P. (2021) · Biomarkers in Neuropsychiatry · doi:10.1016/j.bionps.2021.100041 · Cited by 42
The past, present, and future of disease-modifying therapies for Alzheimer’s disease
Suzuki, K., Iwata, A., & Iwatsubo, T. (2017) · Proceedings of the Japan Academy Series B · doi:10.2183/pjab.93.048 · Cited by 42
Roe, C. M., Ances, B. M., Head, D. M., Babulal, G. M., Stout, S. H., Grant, E., Hassenstab, J. J., Xiong, C., Holtzman, D. M., Benzinger, T. L. S., et al. (2018) · Brain · doi:10.1093/brain/awy244 · Cited by 42
Self-citationTimmers, M., Tesseur, I. C., Bogert, J., Zetterberg, H., Blennow, K., Börjesson‐Hanson, A., Baquero, M., Boada, M., RANDOLPH, C. C., Tritsmans, L., et al. (2019) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2019.03.016 · Cited by 43
Plasma lipocalin‐2 levels in the preclinical stage of Alzheimer's disease
Eruysal, E., Ravdin, L., Kamel, H., Iadecola, C., & Ishii, M. (2019) · Alzheimer s & Dementia Diagnosis Assessment & Disease Monitoring · doi:10.1016/j.dadm.2019.07.004 · Cited by 42
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“However, the high expense and limited availability of the amyloid PET and the invasive nature of CSF collection highly limit its wide used in clinic practice (Villemagne et al., 2013; Vos et al., 2013; Sperling et al., 2014; Baird et al., 2015).”
BackgroundProgressive medial temporal lobe atrophy during preclinical Alzheimer's disease
Pettigrew, C. A., Soldan, A., Sloane, K. L., Cai, Q., Wang, J., Wang, M., Moghekar, A., Miller, M. I., & Albert, M. (2017) · NeuroImage Clinical · doi:10.1016/j.nicl.2017.08.022 · Cited by 39
“The resulting proportion of individuals classified into the four CSF groups was very comparable to prior studies that used clinically validated cut-points (e.g., Jack et al., 2017; Mormino et al., 2014; Vos et al., 2013).”
ResultCSF beta‐amyloid 1–42 – what are we measuring in Alzheimer's disease?
Hu, W. T., Watts, K. D., Shaw, L. M. J., Howell, J. C., Trojanowski, J. Q., Basra, S. S., Glass, J. D., Lah, J. J., & Levey, A. I. (2014) · Annals of Clinical and Translational Neurology · doi:10.1002/acn3.160 · Cited by 38
Circadian Rhythms in AD Pathogenesis: a Critical Appraisal
Musiek, E. S. (2017) · Current Sleep Medicine Reports · doi:10.1007/s40675-017-0072-5 · Cited by 37
Berman, S. E., Koscik, R. L., Clark, L. R., Mueller, K. D., Bluder, L., Galvin, J. E., & Johnson, S. C. (2017) · Journal of Alzheimer s Disease Reports · doi:10.3233/adr-170004 · Cited by 38
Imaging Translocator Protein as a Biomarker of Neuroinflammation in Dementia
Kreisl, W. C., Henter, I. D., & Innis, R. B. (2017) · Advances in pharmacology · doi:10.1016/bs.apha.2017.08.004 · Cited by 41
“In addition, MCI patients without evidence of amyloidopathy are less likely to have pathologically defined AD at autopsy (Vos et al., 2013), and they show less cognitive decline than amyloid-positive MCI patients (Landau, Horng, Fero, Jagust, & Alzheimer’s Adv Pharmacol.”
BackgroundWirth, M., Bejanin, A., Joie, R. L., Arenaza‐Urquijo, E. M., Gonneaud, J., Landeau, B., Perrotin, A., Mézenge, F., Sayette, V. D. L., Desgranges, B., et al. (2017) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2017.10.023 · Cited by 40
Altered structural network organization in cognitively normal individuals with amyloid pathology
Voevodskaya, O., Pereira, J. B., Volpe, G., Lindberg, O. E., Stomrud, E., van Westen, D., Westman, E., & Hansson, O. (2017) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2017.11.014 · Cited by 41
“Several studies have shown that asymptomatic individuals with evidence of cerebral amyloidosis have an increased risk of subsequent cognitive decline, including development of AD dementia (Insel et al., 2016; Jagust, 2016; Vos et al., 2013).”
BackgroundOcular Biomarkers of Alzheimer's Disease: The Role of Anterior Eye and Potential Future Directions
Dehghani, C., Frost, S. M., Jayasena, R., Masters, C. L., & Kanagasingam, Y. (2018) · Investigative Ophthalmology & Visual Science · doi:10.1167/iovs.18-24694 · Cited by 37
Thirunavu, V. M., McCullough, A. A., Su, Y., Flores, S. E., Dincer, A., Morris, J. C., Cruchaga, C., Benzinger, T. L. S., & Gordon, B. A. (2019) · Journal of Alzheimer s Disease · doi:10.3233/jad-190154 · Cited by 37
Self-citationElevated serum creatine kinase in the early stage of sporadic amyotrophic lateral sclerosis
Ito, D., Hashizume, A., Hijikata, Y., Yamada, S., Iguchi, Y., Iida, M., Kishimoto, Y., Moriyoshi, H., Hirakawa, A., & Katsuno, M. (2019) · Journal of Neurology · doi:10.1007/s00415-019-09507-6 · Cited by 37
Aschenbrenner, A. J., Balota, D. A., Fagan, A. M., Duchek, J. M., Benzinger, T. L. S., & Morris, J. C. (2015) · Journal of the International Neuropsychological Society · doi:10.1017/s1355617715000776 · Cited by 37
“For descriptive purposes, we have indicated the proportion of individuals with “abnormal”Aβ42 and tau based on recently published cut offs (Vos et al., 2013) although we use the continuous measures for the current analyses.”
MethodSelf-citationKuller, L. H., López, O. L., Becker, J. T., Chang, Y., & Newman, A. B. (2015) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2015.08.165 · Cited by 41
“A second hypothesis is that dementia in the very old is a result of brain amyloid disease with a long incubation period, secondary neurodegeneration [53–55].”
Braak stage and trajectory of cognitive decline in noncognitively impaired elders
Mufson, E. J., Malek‐Ahmadi, M. H., Snyder, N. L., Ausdemore, J., Chen, K., & Perez, S. E. (2016) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2016.03.003 · Cited by 38
“…indicate that cognitively normal ε4 carriers are more likely to have significant AD-related pathology M AN US CR IP T AC CE PT ED ACCEPTED MANUSCRIPT 13 relative to non-carriers, but rates of cognitive decline were not significantly different between carriers and non-carriers (Vos et al., 2013).”
BackgroundResultUse of ocular biomarkers as a potential tool for early diagnosis of Alzheimer's disease
Singh, A., & Verma, S. (2020) · Indian Journal of Ophthalmology · doi:10.4103/ijo.ijo_999_19 · Cited by 36
Quevenco, F. C., Bergen, J. M. G. V., Treyer, V., Studer, S. T., Kagerer, S. M., Meyer, R., Gietl, A. F., Kaufmann, P. A., Nitsch, R. M., Höck, C., et al. (2020) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2020.00046 · Cited by 34
“Several studies demonstrated the validity of positron-emission-tomography (PET) tracers for inferring the relationship between AD-pathology burden, and risk for severe cognitive impairment at old age (Klunk, 2011; Villemagne et al., 2011; Vos et al., 2013).”
BackgroundBiomarkers and cognitive endpoints to optimize trials in Alzheimer's disease
Insel, P. S., Mattsson, N., Mackin, R. S., Kornak, J., Nosheny, R. L., Tosun, D., Donohue, M., Aisen, P. S. S., Weiner, M. W., & Initiative, A. D. N. (2015) · Annals of Clinical and Translational Neurology · doi:10.1002/acn3.192 · Cited by 34
Zhao, Y., Tudorascu, D., López, O. L., Cohen, A. D., Mathis, C. A., Aizenstein, H. J., Price, J. C., Kuller, L. H., Kamboh, M. I., DeKosky, S. T., et al. (2017) · JAMA Neurology · doi:10.1001/jamaneurol.2017.3029 · Cited by 35
Bos, I., Vos, S. J. B., Jansen, W. J., Vandenberghe, R. R., Gabel, S., Estanga, A., Ecay‐Torres, M., Tomassen, J., den Braber, A., Lleó, A., et al. (2018) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2018.00193 · Cited by 35
Self-citationPathological drivers of neurodegeneration in suspected non-Alzheimer’s disease pathophysiology
Wisse, L. E. M., de Florès, R., Xie, L., Das, S. R., McMillan, C. T., Trojanowski, J. Q., Grossman, M., Lee, E. B., Irwin, D. J., Yushkevich, P. A., et al. (2021) · Alzheimer s Research & Therapy · doi:10.1186/s13195-021-00835-2 · Cited by 37
“These findings line up with previous studies of neuropathological diagnoses in SNAP reporting a low prevalence of AD [31, 32] but supporting the presence of PART, AGD, and LBD [32, 33].”
ResultThe role of positron emission tomography imaging in understanding Alzheimer’s disease
Barthel, H., Seibyl, J. P., & Sabri, O. (2015) · Expert Review of Neurotherapeutics · doi:10.1586/14737175.2015.1023296 · Cited by 34
“In another recent longitudinal cohort study including 311 cognitively normal subjects older than 65 years, a suspected non-AD pathology frequency of 23% was reported [17].”
BackgroundMorphometric Changes to Corneal Dendritic Cells in Individuals With Mild Cognitive Impairment
Dehghani, C., Frost, S. M., Jayasena, R., Fowler, C. J., Masters, C. L., Kanagasingam, Y., Jiao, H., Lim, J. K. H., Chinnery, H. R., & Downie, L. E. (2020) · Frontiers in Neuroscience · doi:10.3389/fnins.2020.556137 · Cited by 34
“Cerebrospinal fluid biomarkers and amyloid PET, which can detect earlier AD pathology, have revealed subtle subclinical pathological changes that occur before the clinical decline (Villemagne et al., 2011, 2013; Vos et al., 2013).”
BackgroundDang, C., Harrington, K. D., Lim, Y. Y., Ames, D., Hassenstab, J., Laws, S. M., Yassi, N., Hickey, M., Rainey-Smith, S., Robertson, J., et al. (2018) · Journal of Alzheimer’s Disease · doi:10.3233/jad-180507 · Cited by 31
“Similarly, estimates of progression at 5 years were based on 25% of the baseline MCSA sample [10], and 35% of the Knight ADRC data were available beyond 5 years [17].”
Self-citationInsel, P. S., Donohue, M., Mackin, R. S., Aisen, P. S. S., Hansson, O., Weiner, M. W., & Mattsson, N. (2016) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2016.08.017 · Cited by 35
“…AD (Sperling et al., 2011b), where subjects with a combination of positive AD biomarkers (including A b biomarkers) and subtle cognitive dysfunction are thought to be at much higher risk for future clinical deterioration compared to subjects with positive A b biomarkers alone (Vos et al., 2013).”
Schreiber, S., Schreiber, F., Lockhart, S. N., Horng, A., Bejanin, A., Landau, S. M., Jagust, W. J., & Initiative, A. D. N. (2017) · JAMA Neurology · doi:10.1001/jamaneurol.2016.5349 · Cited by 33
Millar, P. R., Ances, B. M., Gordon, B. A., Benzinger, T. L. S., Fagan, A. M., Morris, J. C., & Balota, D. A. (2020) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2020.08.007 · Cited by 30
“Specifically, we did not exclude Aβ42-negative participants with elevated pTau, which might reflect suspected non-Alzheimer pathophysiology (SNAP; Vos et al., 2013).”
BackgroundSelf-citationBrugulat‐Serrat, A., Rojas, S., Bargalló, N., Conesa, G., Minguillón, C., Fauria, K., Gramunt, N., Molinuevo, J. L., & Gispert, J. D. (2017) · BMJ Open · doi:10.1136/bmjopen-2016-013215 · Cited by 33
Yang, Y., Hsu, K.-C., Wei, C., Tzeng, R.-C., & Chiu, P. (2021) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2021.705782 · Cited by 36
Circular RNAs in Alzheimer’s Disease: A New Perspective of Diagnostic and Therapeutic Targets
Vakili, O., Asili, P., Babaei, Z., Mirahmad, M., Keshavarzmotamed, A., Asemi, Z., & Mafi, A. (2022) · CNS & Neurological Disorders - Drug Targets · doi:10.2174/1871527321666220829164211 · Cited by 34
CSF Alzheimer Disease Biomarkers
Greenberg, B., Pettigrew, C. A., Soldan, A., Wang, J., Wang, M., Darrow, J. A., Albert, M., & Moghekar, A. (2022) · Neurology · doi:10.1212/wnl.0000000000200953 · Cited by 32
A sandwich immunoassay for detection of Aβ1-42 based on quantum dots
Pi, J., Long, Y., Huang, N., Cheng, Y. Z., & Zheng, H. (2015) · Talanta · doi:10.1016/j.talanta.2015.08.022 · Cited by 31
Mar, J., Soto‐Gordoa, M., Arrospide, A., Moreno, F., & Martínez‐Lage, P. (2015) · Alzheimer s Research & Therapy · doi:10.1186/s13195-014-0079-9 · Cited by 31
“The size of these target populations constrains the viability of an ideal public health perspective to reduce AD prevalence based on a scalable approach, with interventions first targeting risk factors and then pharmacologic treatment in a highly selected group of individuals [9].”
BackgroundHarrington, K., Lim, Y. Y., Ames, D. J., Hassenstab, J. J., Laws, S. M., Martins, R. N., Rainey‐Smith, S. R., Robertson, J. S., Rowe, C. C., Salvado, O., et al. (2017) · Alzheimer s & Dementia Diagnosis Assessment & Disease Monitoring · doi:10.1016/j.dadm.2017.05.006 · Cited by 33
“8% in Australian Imaging Biomarkers and Lifestyle [AIBL] [3], 10% in Knight Alzheimer’s Disease Research Centre [Knight ADRC] [9], 7.”
BackgroundInfluentialSelf-citationFlavonoids and Alzheimer’s disease: reviewing the evidence for neuroprotective potential
Amin, M. A., Dehbia, Z., Nafady, M. H., Zehravi, M., Kumar, K. P., Haque, M. A., Baig, M. S., Farhana, A., Khan, S. L., Afroz, T., et al. (2024) · Molecular and Cellular Biochemistry · doi:10.1007/s11010-023-04922-w · Cited by 29
“According to the study, a buildup alone is likely insufficient to cause symptoms [30–32].”
Huszár, Z., Engh, M. A., Pavlekovics, M., Sato, T., Steenkamp, Y., Hanseeuw, B. J., Terebessy, T., Molnár, Z., Hegyi, P., & Csukly, G. (2024) · Alzheimer s Research & Therapy · doi:10.1186/s13195-024-01455-2 · Cited by 30
Integrative Single-Plaque Analysis Reveals Signature Aβ and Lipid Profiles in the Alzheimer’s Brain
Enzlein, T., Lashley, T., Sammour, D. A., Hopf, C., & Chávez‐Gutiérrez, L. (2024) · Analytical Chemistry · doi:10.1021/acs.analchem.3c05557 · Cited by 28
Fractal motor activity regulation and sex differences in preclinical Alzheimer's disease pathology
Gao, L., Li, P., Gaba, A., Musiek, E. S., Ju, Y. S., & Hu, K. (2021) · Alzheimer s & Dementia Diagnosis Assessment & Disease Monitoring · doi:10.1002/dad2.12211 · Cited by 29
12-year prediction of mild cognitive impairment aided by Alzheimer’s brain signatures at mean age 56
Williams, M. E., Elman, J. A., McEvoy, L. K., Andreassen, O. A., Dale, A. M., Eglit, G. M. L., Eyler, L. T., Fennema‐Notestine, C., Franz, C. E., Gillespie, N. A., et al. (2021) · Brain Communications · doi:10.1093/braincomms/fcab167 · Cited by 29
Baldeiras, I., Santana, I. J., Leitão, M. J., Ribeiro, M. H., Pascoal, R., Duro, D., Lemos, R., Santiago, B., Almeida, M. R., & Oliveira, C. R. (2015) · Journal of the Neurological Sciences · doi:10.1016/j.jns.2015.09.022 · Cited by 30
Biomarker-based signature of alzheimer's disease in pre-MCI individuals
Chipi, E., Salvadori, N., Farotti, L., & Parnetti, L. (2019) · Brain Sciences · doi:10.3390/brainsci9090213 · Cited by 27
“25 SD (lowest tenth percentile of the distribution in the group) in episodic memory composite score and a Clinical Dementia Rating (CDR) score of 0 were applied to signify subtle cognitive decline in preclinical AD stage 3 [51].”
MethodJoannette, M., Bocti, C., Sévigny-Dupont, P., Lavallée, M. M., Nikelski, J., Vallet, G. T., Chertkow, H. M., & Joubert, S. (2019) · The Journals of Gerontology Series A · doi:10.1093/gerona/glz235 · Cited by 27
“Aβ begins to accumulate before the first clinical signs of AD and is associated with an increased risk for future cognitive decline (7,8).”
BackgroundJang, H., Kim, H. J., Park, S., Park, Y. H., Choe, Y. S., Cho, H., Lyoo, C. H., Yoon, U., Lee, J. S., Kim, Y., et al. (2019) · European Journal of Nuclear Medicine and Molecular Imaging · doi:10.1007/s00259-019-04498-y · Cited by 27
Knopman, D. S., Jack, C. R., Lundt, E. S., Weigand, S. D., Vemuri, P., Lowe, V. J., Kantarci, K., Gunter, J. L., Senjem, M. L., Mielke, M. M., et al. (2016) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2016.06.003 · Cited by 27
“…progression both from CN to MCI (Knopman et al., 2012; Mormino et al., 2014; Roe et al., 2013; Toledo et al., 2014; van Harten et al., 2013; Vos et al., 2013; Wirth et al., 2013) or from MCI to dementia (Caroli et al., 2015; Petersen et al., 2013; Prestia et al., 2013; van Rossum et al.,…”
BackgroundPeripheral Neuropathy Research Registry: A prospective cohort
Thomas, S., Ajroud‐Driss, S., Dimachkie, M. M., Gibbons, C. H., Freeman, R. L., Simpson, D. M., Singleton, J. R., Smith, A. G., PNRR Study Group, & Höke, A. (2019) · Journal of the Peripheral Nervous System · doi:10.1111/jns.12301 · Cited by 26
“Based on cohorts for other neurodegenerative diseases, 3 – 5 we established a prospective cohort of acquired axonal PN patients, including those with small fiber neuropathies (defined as a sub-group of axonal neuropathies with only small fiber symptoms and/or abnormal epidermal nerve fiber…”
Choriocapillaris and Retinal Vascular Alterations in Presymptomatic Alzheimer's Disease
Corradetti, G., Oncel, D., Kadomoto, S., Arakaki, X., Kloner, R. A., Sadun, A. A., Sadda, S. R., & Chan, J. W. (2024) · Investigative Ophthalmology & Visual Science · doi:10.1167/iovs.65.1.47 · Cited by 26
Jacquemont, T., Fallani, F. D. V., Bertrand, A., Epelbaum, S., Routier, A., Dubois, B., Hampel, H. J., Durrleman, S., & Olivier Colliot, A. (2017) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2017.03.023 · Cited by 26
“This population has been shown to display a high rate of APOE ε4 carriers, a greater cognitive decline over time and a higher rate of progression and conversion to AD (Caroli et al., 2015; Edmonds et al., 2015; Knopman et al., 2012; Prestia et al., 2013; Vos et al., 2013).”
BackgroundResultRole of Body-Fluid Biomarkers in Alzheimer’s Disease Diagnosis
Nguyen, T. T., Ta, Q. T. H., Nguyen, T. K. O., Nguyen, T. K. O., & Giau, V. V. (2020) · Diagnostics · doi:10.3390/diagnostics10050326 · Cited by 25
Ishii, M., Kamel, H., & Iadecola, C. (2018) · Journal of Alzheimer s Disease · doi:10.3233/jad-180682 · Cited by 24
“Using previously defined CSF criteria for preclinical AD [14], 20 male and 18 female subjects were categorized as being in the preclinical stage of AD, and 45 male and 73 female subjects were categorized as amyloid-negative controls.”
InfluentialSutoko, S., Masuda, A., Kandori, A., Sasaguri, H., Saito, T., Saido, T. C., & Funane, T. (2021) · iScience · doi:10.1016/j.isci.2021.102198 · Cited by 23
Oberstein, T. J., Schmidt, M. A., Florvaag, A., Haas, A.-L., Siegmann, E.-M., Olm, P., Utz, J., Spitzer, P., Doerfler, A., Lewczuk, P., et al. (2022) · Brain · doi:10.1093/brain/awac297 · Cited by 25
“26,29 The performance at baseline and the cognitive trajectories of the A–”
Predicting Regional Pattern of Longitudinal β-Amyloid Accumulation by Baseline PET
Guo, T., Brendel, M., Grimmer, T., Rominger, A., & Yakushev, I. Y. (2016) · Journal of Nuclear Medicine · doi:10.2967/jnumed.116.176115 · Cited by 24
Aschenbrenner, A. J., Gordon, B. A., Fagan, A. M., Schindler, S. E., Balota, D. A., Morris, J. C., & Hassenstab, J. J. (2020) · Journal of Alzheimer s Disease · doi:10.3233/jad-200018 · Cited by 23
“Includinganindicator ofsubtlecognitivechangealsoincreasespredictive power of disease progression [4].”
Self-citationRacial differences in longitudinal Alzheimer's disease biomarkers among cognitively normal adults
Xiong, C., Luo, J. R., Schindler, S. E., Fagan, A. M., Benzinger, T. L. S., Hassenstab, J. J., Balls‐Berry, J. E., Agboola, F., Grant, E., Moulder, K. L., et al. (2022) · Alzheimer s & Dementia · doi:10.1002/alz.12608 · Cited by 23
Self-citationTudela, R., Muñoz‐Moreno, E., Sala‐Llonch, R., López-Gil, X., & Sòria, G. (2019) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2019.00213 · Cited by 23
“Evidences of early brain changes associated to AD have been suggested decades prior to its clinical diagnosis (Sperling et al., 2011; Vos et al., 2013; Dubois et al., 2016) but the late appearance of AD symptoms hinders the study of the disease progression in human cohorts.”
BackgroundDicks, E., van der Flier, W. M., Scheltens, P., Barkhof, F., & Tijms, B. M. (2020) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2020.05.008 · Cited by 25
“Individuals with preclinical AD are at increased risk for cognitive decline (Donohue et al., 2017; Parnetti et al., 2019; Vos et al., 2013).”
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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