Gantenerumab reduces amyloid-β plaques in patients with prodromal to moderate Alzheimer’s disease: a PET substudy interim analysis
Open accessAbstract
Background: We previously investigated low doses (105 or 225 mg) of gantenerumab, a fully human monoclonal antibody that binds and removes aggregated amyloid-β by Fc receptor-mediated phagocytosis, in the SCarlet RoAD (SR) and Marguerite RoAD (MR) phase 3 trials. Several lines of evidence suggested that higher doses may be necessary to achieve clinical efficacy. We therefore designed a positron emission tomography (PET) substudy to evaluate the effect of gantenerumab uptitrated to 1200 mg every 4 weeks on amyloid-β plaques as measured using florbetapir PET in patients with prodromal to moderate Alzheimer’s disease (AD). Methods: A subset of patients enrolled in the SR and MR studies who subsequently entered the open-label extensions (OLEs) were included in this substudy. Patients were aged 50 to 90 years with a clinical diagnosis of probable prodromal to moderate AD and were included based on a visual read of the original screening scan in the double-blind phase. Patients were assigned to 1 of 5 titration schedules (ranging from 2 to 10 months) with a target gantenerumab dose of 1200 mg every 4 weeks. The main endpoint of this substudy was change in amyloid-β plaque burden from OLE baseline to week 52 and week 104, assessed using florbetapir PET. Florbetapir global cortical signal was calculated using a prespecified standard uptake value ratio method converted to the Centiloid scale. Results: Sixty-seven of the 89 patients initially enrolled had ≥ 1 follow-up scan by August 15, 2018. Mean amyloid levels were reduced by 39 Centiloids by the first year and 59 Centiloids by year 2, a 3.5-times greater reduction than was seen after 2 years at 225 mg in SR. At years 1 and 2, 37% and 51% of patients, respectively, had amyloid-β plaque levels below the amyloid-β positivity threshold. Conclusion: Results from this exploratory interim analysis of the PET substudy suggest that gantenerumab doses up to 1200 mg resulted in robust amyloid-β plaque removal at 2 years. PET amyloid levels were consistent with sparse-to-no neuritic amyloid-β plaques in 51% of patients after 2 years of therapy. Amyloid reductions were similar to those observed in other placebo-controlled studies that have suggested potential clinical benefit. Trial registration: ClinicalTrials.gov, NCT01224106 (SCarlet RoAD) and NCT02051608 (Marguerite RoAD).
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Amyloid plaque burden must be lowered to approximately 20 centiloids for a significant clinical benefit to become apparent.
“amyloid plaque would need to be reduced to a low level (~20 centiloids) to reveal significant clinical benefit”
From The amyloid hypothesis in Alzheimer disease: new insights from new therapeutics (2022) · cites this paper as [89]
In cognitively unimpaired subjects, there is no meaningful increase in tau PET signal below 22 centiloids, although a 20% increase in amyloid PET SUVr up to about 35 centiloids was associated with a statistically significant increase in annualized tau PET signal.
“Jack et al. 89 have shown there is no meaningful increase in tau PET signal in cognitively unimpaired subjects below 22 CL, although an increase amyloid PET SUVr signal of 20% (up to ~35 CL) was associated with a statistically significant increase in annualized tau PET signal.”
From The amyloid hypothesis in Alzheimer disease: new insights from new therapeutics (2022) · cites this paper as [89]
Gantenerumab was found to be safe and well tolerated during Phase 1 clinical trials, except transient amyloid-related imaging abnormalities (ARIA) appeared in some patients given a high dosage.
“The antibody was found to be safe and well tolerated during the Phase 1 clinical trials, except that transient amyloid-related imaging abnormalities (ARIA) appeared in some patients given a high dosage.336”
From Amyloid β-based therapy for Alzheimer’s disease: Challenges, successes and future (2023) · cites this paper as [336]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Cites
Wang, H., Naghavi, M., Allen, C., Barber, R. M., Bhutta, Z. A., Carter, A., Casey, D. C., Charlson, F. J., Chen, A. Z., Coates, M. M., et al. (2016) · The Lancet · doi:10.1016/s0140-6736(16)31012-1 · Cited by 6,596 · see citing works
The amyloid hypothesis of Alzheimer's disease at 25 years
Selkoe, D. J., & Hardy, J. (2016) · EMBO Molecular Medicine · doi:10.15252/emmm.201606210 · Cited by 6,164 · see citing works
Soluble protein oligomers in neurodegeneration: lessons from the Alzheimer's amyloid β-peptide
Haass, C., & Selkoe, D. J. (2007) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2101 · Cited by 4,744 · see citing works
Clinical and biomarker changes in dominantly inherited Alzheimer's disease
Bateman, R. J., Xiong, C., Benzinger, T. L. S., Fagan, A. M., Goate, A., Fox, N. C., Marcus, D. S., Cairns, N. J., Xie, X., Blazey, T. M., et al. (2012) · New England Journal of Medicine · doi:10.1056/nejmoa1202753 · Cited by 3,814 · see citing works
Self-citationThe antibody aducanumab reduces Aβ plaques in Alzheimer’s disease
Sevigny, J., Chiao, P., Bussière, T., Weinreb, P. H., Williams, L., Maier, M., Dunstan, R., Salloway, S., Chen, T., Ling, Y., et al. (2016) · Nature · doi:10.1038/nature19323 · Cited by 3,059 · see citing works
Villemagne, V. L., Burnham, S., Bourgeat, P., Brown, B., Ellis, K. A., Salvado, O., Szoeke, C., Macaulay, S. L., Martins, R., Maruff, P., et al. (2013) · The Lancet Neurology · doi:10.1016/s1474-4422(13)70044-9 · Cited by 2,279 · see citing works
The cholinergic hypothesis of Alzheimer’s disease: A review of progress
Francis, P. T., Palmer, A. M., Snape, M., & Wilcock, G. K. (1999) · Journal of Neurology, Neurosurgery & Psychiatry · doi:10.1136/jnnp.66.2.137 · Cited by 2,198 · see citing works
The toxic Aβ oligomer and Alzheimer's disease: an emperor in need of clothes
Benilova, I., Karran, E., & De Strooper, B. (2012) · Nature Neuroscience · doi:10.1038/nn.3028 · Cited by 1,962 · see citing works
Cholinesterase inhibitors for Alzheimer's disease
Birks, J. S. (2006) · Cochrane Database of Systematic Reviews · doi:10.1002/14651858.cd005593 · Cited by 1,906 · see citing works
The Centiloid Project: standardizing quantitative amyloid plaque estimation by PET
Klunk, W. E., Koeppe, R. A., Price, J. C., Benzinger, T. L., Devous, M. D., Jagust, W. J., Johnson, K. A., Mathis, C. A., Minhas, D., Pontecorvo, M. J., et al. (2015) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2014.07.003 · Cited by 1,348 · see citing works
Use of Florbetapir-PET for Imaging β-Amyloid Pathology
Clark, C. M. (2011) · JAMA · doi:10.1001/jama.2010.2008 · Cited by 1,117 · see citing works
Clark, C. M., Pontecorvo, M. J., Beach, T. G., Bedell, B. J., Coleman, R. E., Doraiswamy, P. M., Fleisher, A. S., Reiman, E. M., Sabbagh, M. N., Sadowsky, C. H., et al. (2012) · The Lancet Neurology · doi:10.1016/s1474-4422(12)70142-4 · Cited by 855 · see citing works
Randomized trial of verubecestat for mild-to-moderate Alzheimer's disease
Egan, M. F., Kost, J., Tariot, P. N., Aisen, P. S., Cummings, J. L., Vellas, B., Sur, C., Mukai, Y., Voss, T., Furtek, C., et al. (2018) · New England Journal of Medicine · doi:10.1056/nejmoa1706441 · Cited by 685 · see citing works
Barthel, H., Gertz, H., Dresel, S. H. J., Peters, O., Bartenstein, P., Büerger, K., Hiemeyer, F. J., Wittemer‐Rump, S., Seibyl, J. P., Reininger, C. B., et al. (2011) · The Lancet Neurology · doi:10.1016/s1474-4422(11)70077-1 · Cited by 588 · see citing works
A phase III randomized trial of gantenerumab in prodromal Alzheimer’s disease
for the SCarlet RoAD Investigators, Ostrowitzki, S., Lasser, R. A., Dorflinger, E., Scheltens, P., Barkhof, F., Nikolcheva, T., Ashford, E., Retout, S., Hofmann, C., et al. (2017) · Alzheimer's Research & Therapy · doi:10.1186/s13195-017-0318-y · Cited by 567 · see citing works
Self-citationDonepezil for dementia due to Alzheimer's disease
Birks, J., & Harvey, R. J. (2003) · Cochrane Database of Systematic Reviews · doi:10.1002/14651858.cd001190 · Cited by 515 · see citing works
Bohrmann, B., Baumann, K., Benz, J., Gerber, F., Huber, W., Knoflach, F., Messer, J., Oroszlan, K., Rauchenberger, R., Richter, W. F., et al. (2012) · Journal of Alzheimer's Disease · doi:10.3233/jad-2011-110977 · Cited by 448 · see citing works
Mechanism of amyloid removal in patients with Alzheimer disease treated with gantenerumab
Ostrowitzki, S. (2012) · Archives of Neurology · doi:10.1001/archneurol.2011.1538 · Cited by 431 · see citing works
Joshi, A. D., Pontecorvo, M. J., Clark, C. M., Carpenter, A. P., Jennings, D. L., Sadowsky, C., Adler, L. P., Kovnat, K. D., Seibyl, J. P., Arora, A., et al. (2012) · Journal of Nuclear Medicine · doi:10.2967/jnumed.111.090340 · Cited by 391 · see citing works
Kennedy, M., Stamford, A., Chen, X., Cox, K., Cumming, J., Dockendorf, M., Egan, M. F., Ereshefsky, L., Hodgson, R., Hyde, L., et al. (2016) · Science Translational Medicine · doi:10.1126/scitranslmed.aad9704 · Cited by 391 · see citing works
Phase 3 solanezumab trials: Secondary outcomes in mild Alzheimer's disease patients
Siemers, E. R., Sundell, K. L., Carlson, C., Case, M., Sethuraman, G., Liu‐Seifert, H., Dowsett, S. A., Pontecorvo, M. J., Dean, R. A., & Demattos, R. (2016) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2015.06.1893 · Cited by 370 · see citing works
Fleisher, A. S. (2011) · Archives of Neurology · doi:10.1001/archneurol.2011.150 · Cited by 364 · see citing works
Galantamine for Alzheimer's disease and mild cognitive impairment
Loy, C. T., & Schneider, L. S. S. (2006) · Cochrane Database of Systematic Reviews · doi:10.1002/14651858.cd001747.pub3 · Cited by 335 · see citing works
Thomas, B. A., Erlandsson, K., Marc Modat, A., Thurfjell, L., Vandenberghe, R. R., Sebastien Ourselin, A., & Hutton, B. F. (2011) · European Journal of Nuclear Medicine and Molecular Imaging · doi:10.1007/s00259-011-1745-9 · Cited by 317 · see citing works
Cummings, J. L., Cohen, S., van Dyck, C. H., Brody, M., Curtis, C. T., Cho, W., Ward, M. E., Friesenhahn, M. J., Rabe, C., Brunstein, F., et al. (2018) · Neurology · doi:10.1212/wnl.0000000000005550 · Cited by 253 · see citing works
Partial volume correction in quantitative amyloid imaging
Su, Y., Blazey, T. M., Snyder, A. Z., Raichle, M. E., Marcus, D. S., Ances, B. M., Bateman, R. J., Cairns, N. J., Aldea, P., Cash, L., et al. (2015) · NeuroImage · doi:10.1016/j.neuroimage.2014.11.058 · Cited by 247 · see citing works
Self-citationSoluble forms of tau are toxic in Alzheimer's disease
Kopeikina, K., Hyman, B., & Spires-Jones, T. (2012) · Translational Neuroscience · doi:10.2478/s13380-012-0032-y · Cited by 232 · see citing works
Navitsky, M., Joshi, A. D., Kennedy, I., Klunk, W. E., Rowe, C. C., Wong, D. F., Pontecorvo, M. J., Mintun, M. A., & Devous, M. D. (2018) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2018.06.1353 · Cited by 229 · see citing works
Longitudinal Amyloid Imaging Using 11C-PiB: Methodologic Considerations
van Berckel, B. N. M., Ossenkoppele, R., Tolboom, N., Yaqub, M. M., Foster‐Dingley, J. C., Windhorst, A. D., Scheltens, P., Lammertsma, A. A., & Boellaard, R. (2013) · Journal of Nuclear Medicine · doi:10.2967/jnumed.112.113654 · Cited by 163 · see citing works
Schmidt, M. E., Chiao, P., Klein, G., Matthews, D. C., Thurfjell, L., Cole, P. E., Margolin, R. A., Landau, S. M., Foster, N. L., Mason, N. S., et al. (2014) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2014.09.004 · Cited by 125 · see citing works
Self-citationAmyloid PET Screening for Enrichment of Early-Stage Alzheimer Disease Clinical Trials
Sevigny, J., Suhy, J., Chiao, P., Chen, T., Klein, G., Purcell, D. D., Oh, J., Verma, A., Sampat, M. P., & Barakos, J. A. (2016) · Alzheimer Disease & Associated Disorders · doi:10.1097/wad.0000000000000144 · Cited by 114 · see citing works
Self-citationA Comparison of Partial Volume Correction Techniques for Measuring Change in Serial Amyloid PET SUVR
Schwarz, C. G., Gunter, J. L., Lowe, V. J., Weigand, S. D., Vemuri, P., Senjem, M. L., Petersen, R. C., Knopman, D. S., & Jack, C. R. (2018) · Journal of Alzheimer s Disease · doi:10.3233/jad-180749 · Cited by 85 · see citing works
Current Treatment and Recent Clinical Research in Alzheimer's Disease
Neugroschl, J. A., & Sano, M. (2010) · Mount Sinai Journal of Medicine A Journal of Translational and Personalized Medicine · doi:10.1002/msj.20165 · Cited by 83 · see citing works
Amyloid Clearance as a Treatment Target Against Alzheimer's Disease
Kurz, A., & Perneczky, R. (2011) · Journal of Alzheimer's Disease · doi:10.3233/jad-2011-102139 · Cited by 78 · see citing works
Villemagne, V. L., Rowe, C. C., Barnham, K. J., Cherny, R. A., Woodward, M., Bozinosvski, S., Salvado, O., Bourgeat, P., Perez, K. A., Fowler, C. J., et al. (2017) · Alzheimer s & Dementia Translational Research & Clinical Interventions · doi:10.1016/j.trci.2017.10.001 · Cited by 72 · see citing works
Delor, I., Charoin, J.-E., Gieschke, R., Retout, S., Jacqmin, P., & Initiative, A. D. N. (2013) · CPT Pharmacometrics & Systems Pharmacology · doi:10.1038/psp.2013.54 · Cited by 57 · see citing works
New and emerging treatments for Alzheimer’s disease
Corbett, A., Smith, J. S., & Ballard, C. G. (2012) · Expert Review of Neurotherapeutics · doi:10.1586/ern.12.43 · Cited by 56 · see citing works
Is Beta-Amyloid Accumulation a Cause or Consequence of Alzheimer's Disease?
Wang, S., Mims, P. N., Roman, R. J., & Fan, F. (2016) · PubMed · Cited by 48 · see citing works
Profile of gantenerumab and its potential in the treatment of Alzheimer's disease
Nisticò, R., Novakovic, D., Feligioni, M., Scaccianoce, S., Piccinin, S., Mercuri, N. B., Nicoletti, F., Caruso, A., Schepisi, C., & Errico, F. (2013) · Drug Design Development and Therapy · doi:10.2147/dddt.s53401 · Cited by 45 · see citing works
Biomarker pattern of ARIA-E participants in phase 3 randomized clinical trials with bapineuzumab
Liu, E., Wang, D., Sperling, R. A., Salloway, S., Fox, N. C., Blennow, K., Scheltens, P., Schmidt, M. E., Streffer, J. R., Novak, G., et al. (2018) · Neurology · doi:10.1212/wnl.0000000000005060 · Cited by 42 · see citing works
Self-citationCselényi, Z., & Farde, L. (2015) · Journal of Cerebral Blood Flow & Metabolism · doi:10.1038/jcbfm.2015.66 · Cited by 34 · see citing works
Brody, M., Liu, E., Di, J., Lu, M., Margolin, R. A., Werth, J. L., Booth, K., Shadman, A., Brashear, H. R., & Novak, G. (2016) · Journal of Alzheimer s Disease · doi:10.3233/jad-160369 · Cited by 32 · see citing works
Swanson, C. J., Zhang, Y., Dhadda, S., Wang, J., Kaplow, J. M., Lai, R. Y. K., Lannfelt, L., Kramer, L. D., & Luthman, J. (2018) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2018.07.009 · Cited by 28 · see citing works
Ottoy, J., Verhaeghe, J. A. J., Niemantsverdriet, E., Engelborghs, S., Stroobants, S. G., & Staelens, S. G. (2017) · PLoS ONE · doi:10.1371/journal.pone.0189155 · Cited by 14 · see citing works
Abi‐Saab, D., Andjelković, M., Pross, N., Delmar, P., Voyle, N., Klein, G., Esau, N., Ristic, S., Martényi, F., da Fontoura, P. P., et al. (2018) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2018.06.2381 · Cited by 8 · see citing works
Self-citationFleisher, A., Lowe, S. L., Liu, P., Shcherbinin, S., Li, L., Chua, L., Nakano, M. H., Hawdon, A., Willis, B. A., Schwarz, A. J., et al. (2018) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2018.06.2378 · Cited by 8 · see citing works
Andjelković, M., Abi‐Saab, D., Delmar, P., Pross, N., Voyle, N., Klein, G., Mertes, M., Ristic, S., Martényi, F., da Fontoura, P. P., et al. (2018) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2018.06.2382 · Cited by 6 · see citing works
Self-citationvon Rosenstiel, P., Gheuens, S., Chen, T., et al. (2018) · Neurology · doi:10.1212/wnl.90.15_supplement.s2.003 · Cited by 5 · see citing works
Flagged first, then by citations
Research works printed but not linked: 4
- [4]Birks JS Melzer D Beppu H Donepezil for mild and moderate Alzheimer’s disease Cochrane Database Syst Rev 2000 4 CD001190 11034704
- [24]Abi-Saab D, Andjelkovic M, Pross N, Delmar P, Voyle N, Esau N, et al. MRI findings in the open label extension of the Marguerite RoAD study in patients with mild Alzheimer’s disease. J Prev Alz Dis. 2017;4:339 (P36).
- [38]Klein G, Delmar P, Abi-Saab D, Andjelkovic M, Milosavljevic-Ristic S, Seibyl J, et al. Methodologic considerations for calculating standard uptake value ratio amyloid reduction in the gantenerumab open label extension studies. Human Amyloid Imaging (HAI) Conference; 2018; Miami, FL, USA.
- [41]Fleisher AS, Lowe SL, Liu P, Shcherbinin S, Li L, Chua L, et al. Safety, tolerability, pharmacokinetics, and pharmacodynamics of single and multiple intravenous doses of LY3002813, a β-amyloid plaque-specific antibody, in patients iwth mild cognitive impairment due to Alzheimer’s Disease or mild to moderate Alzheimer’s Dementia. Alzheimer’s Association International Conference (AAIC); 2018; Chicago.
Cited by
Sorted by citations
Amyloid β-based therapy for Alzheimer’s disease: Challenges, successes and future
Zhang, Y., Chen, H., Li, R., Sterling, K., & Song, W. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01484-7 · Cited by 988 · see citing works
“The antibody was found to be safe and well tolerated during the Phase 1 clinical trials, except that transient amyloid-related imaging abnormalities (ARIA) appeared in some patients given a high dosage.(336) The initial results of phase 2 studies suggested gantenerumab may have no efficacy in the enrolled cohort.”
BackgroundThe amyloid hypothesis in Alzheimer disease: new insights from new therapeutics
Karran, E., & De Strooper, B. (2022) · Nature Reviews Drug Discovery · doi:10.1038/s41573-022-00391-w · Cited by 742 · see citing works
Alzheimer’s disease: Recent treatment strategies
Vaz, M., & Silvestre, S. (2020) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2020.173554 · Cited by 547 · see citing works
Tolar, M., Abushakra, S., Hey, J. A., Porsteinsson, A., & Sabbagh, M. (2020) · Alzheimer's Research & Therapy · doi:10.1186/s13195-020-00663-w · Cited by 354 · see citing works
Jeremic, D., Jiménez-Díaz, L., & Navarro-López, J. D. (2021) · Ageing Research Reviews · doi:10.1016/j.arr.2021.101496 · Cited by 306 · see citing works
Shi, M., Chu, F., Zhu, F., & Zhu, J. (2022) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2022.870517 · Cited by 275 · see citing works
Moving fluid biomarkers for Alzheimer’s disease from research tools to routine clinical diagnostics
Zetterberg, H., & Blennow, K. (2021) · Molecular Neurodegeneration · doi:10.1186/s13024-021-00430-x · Cited by 219 · see citing works
Quantification of amyloid PET for future clinical use: a state-of-the-art review
Pemberton, H. G., Collij, L. E., Heeman, F., Bollack, A., Shekari, M., Salvadó, G., Alves, I. L., Garcia, D. V., Battle, M., Buckley, C., et al. (2022) · European Journal of Nuclear Medicine and Molecular Imaging · doi:10.1007/s00259-022-05784-y · Cited by 226 · see citing works
Aducanumab produced a clinically meaningful benefit in association with amyloid lowering
Cummings, J., Aisen, P., Lemere, C., Atri, A., Sabbagh, M., & Salloway, S. (2021) · Alzheimer's Research & Therapy · doi:10.1186/s13195-021-00838-z · Cited by 224 · see citing works
Anti-amyloid antibody therapies in Alzheimer's disease
Perneczky, R., Jessen, F., Grimmer, T., Levin, J., Flöel, A., Peters, O., & Froelich, L. (2023) · Brain · doi:10.1093/brain/awad005 · Cited by 182 · see citing works
Predicting future rates of tau accumulation on PET
Jack, C. R., Wiste, H. J., Weigand, S. D., Therneau, T. M., Lowe, V. J., Knopman, D. S., Botha, H., Graff-Radford, J., Jones, D. T., Ferman, T. J., et al. (2020) · Brain · doi:10.1093/brain/awaa248 · Cited by 117 · see citing works
Disease-Modifying Therapies for Alzheimer’s Disease: More Questions than Answers
Golde, T. E. (2022) · Neurotherapeutics · doi:10.1007/s13311-022-01201-2 · Cited by 119 · see citing works
Bateman, R. J., Cummings, J., Schobel, S., Salloway, S., Vellas, B., Boada, M., Black, S. E., Blennow, K., Fontoura, P., Klein, G., et al. (2022) · Alzheimer's Research & Therapy · doi:10.1186/s13195-022-01110-8 · Cited by 109 · see citing works
Self-citationAnti-Amyloid Therapies for Alzheimer’s Disease and the Amyloid Cascade Hypothesis
Fedele, E. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms241914499 · Cited by 102 · see citing works
Anti-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 · see citing works
Cao, Y., Yu, F., Lyu, Y., & Lu, X. (2022) · Frontiers in Neurology · doi:10.3389/fneur.2022.1034243 · Cited by 26 · see citing works
- Authors
- Klein, G., Delmar, P., Voyle, N., Rehal, S., Hofmann, C., Abi-Saab, D., Andjelkovic, M., Ristic, S., Wang, G., Bateman, R., Kerchner, G. A., Baudler, M., Fontoura, P., & Doody, R.
- Affiliations
- F. Hoffmann-La Roche AG (CH)
- Roche (United Kingdom) (GB)
- Washington University in St. Louis (US)
- Corresponding author
- Klein, Gregory
- ORCID
- Venue
- Alzheimer's Research & Therapy
- Published
- 2019-12
- Volume
- 11
- Issue
- 1
- Pages
- 101-101
- ISSN
- 1758-9193 (ISSN-L)
- PMC
- PMC6909550
- OpenAlex
- W2995502746
- Cited by
- 212
- References
- 48
- Citations by year
- 2026: 7 · 2025: 22 · 2024: 39 · 2023: 40 · 2022: 50 · 2021: 33 · 2020: 21
- FWCI
- 17.84
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Alzheimer s Research & Therapy (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Digital Commons@Becker (Washington University School of Medicine) (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- F. Hoffmann-La Roche (n/a)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- amyloid plaques, Alzheimer's disease, prodromal Alzheimer's disease, florbetapir PET, amyloid PET, monoclonal antibodies, Fc receptor-mediated phagocytosis, dose titration, amyloid-beta clearance, open-label extension
- MeSH terms
- Aged, Aged, 80 and over, Alzheimer Disease, Brain, Double-Blind Method, Female, Humans, Male, Middle Aged, Treatment Outcome, Positron-Emission Tomography, Plaque, Amyloid, Antibodies, Monoclonal, Humanized
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review