Cited by 431Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

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Mechanism of Amyloid Removal in Patients With Alzheimer Disease Treated With Gantenerumab

Ostrowitzki, Susanne·2012·Archives of Neurology

DOI 10.1001/archneurol.2011.1538

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Abstract

BACKGROUND: Gantenerumab is a fully human anti-Aβ monoclonal antibody in clinical development for the treatment of Alzheimer disease (AD). OBJECTIVES: To investigate whether treatment with gantenerumab leads to a measurable reduction in the level of Aβ amyloid in the brain and to elucidate the mechanism of amyloid reduction. DESIGN: A multicenter, randomized, double-blind, placebo-controlled, ascending-dose positron emission tomographic study. Additionally, ex vivo studies of human brain slices from an independent sample of patients who had AD were performed. SETTING: Three university medical centers. PATIENTS: Patients with mild-to-moderate AD. INTERVENTION: Two consecutive cohorts of patients received 2 to 7 infusions of intravenous gantenerumab (60 or 200 mg) or placebo every 4 weeks. Brain slices from patients who had AD were coincubated with gantenerumab at increasing concentrations and with human microglial cells. MAIN OUTCOME MEASURES: Percent change in the ratio of regional carbon 11-labeled Pittsburgh Compound B retention in vivo and semiquantitative assessment of gantenerumab-induced phagocytosis ex vivo. RESULTS: Sixteen patients with end-of-treatment positron emission tomographic scans were included in the analysis. The mean (95% CI) percent change from baseline difference relative to placebo (n = 4) in cortical brain amyloid level was -15.6% (95% CI, -42.7 to 11.6) for the 60-mg group (n = 6) and -35.7% (95% CI, -63.5 to -7.9) for the 200-mg group (n = 6). Two patients in the 200-mg group showed transient and focal areas of inflammation or vasogenic edema on magnetic resonance imaging scans at sites with the highest level of amyloid reduction. Gantenerumab induced phagocytosis of human amyloid in a dose-dependent manner ex vivo. CONCLUSION: Gantenerumab treatment resulted in a dose-dependent reduction in brain amyloid level, possibly through an effector cell-mediated mechanism of action.

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BackgroundMethodInfluential
A Multifunctional Chemical Agent as an Attenuator of Amyloid Burden and Neuroinflammation in Alzheimer’s Disease
Cho, H., Sharma, A. K., Zhang, Y., Gross, M. L., & Mirica, L. M. (2020) · ACS Chemical Neuroscience · doi:10.1021/acschemneuro.0c00114 · Cited by 53
Crystal structure reveals conservation of amyloid-β conformation recognized by 3D6 following humanization to bapineuzumab
Feinberg, H., Saldanha, J. W., Diep, L., Goel, A. S., Widom, A., Veldman, G. M., Weis, W. I., Schenk, D., & Basi, G. S. (2014) · Alzheimer s Research & Therapy · doi:10.1186/alzrt261 · Cited by 52
“The efforts underway target either different epitopes of Aβ, (for example, Solaneuzumab [75] and Gantenerumab [15]), different species of Aβ (for example, oligomer specific antibodies discovered via a range of technologies [76] [77] [78] versus plaque specific [48]), or engage different mechanisms to effect clearance…”
Influential
Antibody Therapeutics Targeting Aβ and TauPreprint
Gallardo, G., & Holtzman, D. M. (2017) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a024331 · Cited by 55
Effector function of anti-pyroglutamate-3 Aβ antibodies affects cognitive benefit, glial activation and amyloid clearance in Alzheimer’s-like mice
Crehan, H., Liu, B., Kleinschmidt, M., Rahfeld, J., Le, K. X., Caldarone, B. J., Frost, J. L., Hettmann, T., Hutter‐Paier, B., O’Nuallain, B., et al. (2020) · Alzheimer s Research & Therapy · doi:10.1186/s13195-019-0579-8 · Cited by 48
RETRACTED ARTICLE: Superparamagnetic iron oxide nanoparticles conjugated with Aβ oligomer-specific scFv antibody and class A scavenger receptor activator show therapeutic potentials for Alzheimer’s Disease
Liu, X., Zhang, L., Lü, S., Liu, D., Huang, Y., Zhu, J., Zhou, W.-W., Yu, X., & Liu, R. (2020) · Journal of Nanobiotechnology · doi:10.1186/s12951-020-00723-1 · Cited by 51
Retracted
Immunotherapy targeting pyroglutamate-3 Aβ: prospects and challenges
Cynis, H., Frost, J. L., Crehan, H., & Lemere, C. A. (2016) · Molecular Neurodegeneration · doi:10.1186/s13024-016-0115-2 · Cited by 49
“Gantenerumab was further shown to preferentially bind fibrillar Aβ [63].”
Background
Characterization and preclinical evaluation of the cGMP grade DNA based vaccine, AV-1959D to enter the first-in-human clinical trials
Petrushina, I., Hovakimyan, A., Harahap-Carrillo, I. S., Davtyan, H., Antonyan, T., Chailyan, G., Kazarian, K., Antonenko, M., Jullienne, A., Hamer, M. M., et al. (2020) · Neurobiology of Disease · doi:10.1016/j.nbd.2020.104823 · Cited by 48
Future Therapeutics in Alzheimer’s Disease: Development Status of BACE Inhibitors
Evin, G. M. (2016) · BioDrugs · doi:10.1007/s40259-016-0168-3 · Cited by 52
“Results showed efficacy at reducing amyloid burden in the brain, but also serious adverse effects such as inflammation or vasogenic edema in some patients [70].”
Background
Neuroimaging biomarkers in Alzheimer’s disease and other dementias
Villemagne, V. L., & Chételat, G. (2016) · Ageing Research Reviews · doi:10.1016/j.arr.2016.01.004 · Cited by 55
Advances in Brain Amyloid Imaging
Krishnadas, N., Villemagne, V. L., Doré, V., & Rowe, C. C. (2021) · Seminars in Nuclear Medicine · doi:10.1053/j.semnuclmed.2020.12.005 · Cited by 48
Prodromal Alzheimer's Disease Presenting as Cerebral Amyloid Angiopathy-Related Inflammation with Spontaneous Amyloid-Related Imaging Abnormalities and High Cerebrospinal Fluid Anti-Aβ Autoantibodies
Boncoraglio, G. B., Piazza, F., Savoiardo, M., Farina, L., DiFrancesco, J. C., Prioni, S., Tagliavini, F., Parati, E. A., & Giaccone, G. (2015) · Journal of Alzheimer s Disease · doi:10.3233/jad-142376 · Cited by 45
“Similar MRI abnormalities have been subsequently reported in relation to many other anti-amyloid drugs tested in AD patients and during active immunization with full length A [4–6].”
An effective treatment for Alzheimer's disease must consider both amyloid and tau
Lansdall, C. J. (2014) · Bioscience Horizons The International Journal of Student Research · doi:10.1093/biohorizons/hzu002 · Cited by 46
“is currently assessing a monoclonal antibody that recognizes Aβ, gantenerumab, in patients within the prodromal phase (Ostrowitzki et al., 2012).”
Background
A subcutaneous cellular implant for passive immunization against amyloid-β reduces brain amyloid and tau pathologies
Lathuilière, A., Laversenne, V., Astolfo, A., Kopetzki, E., Jacobsen, H., Stampanoni, M., Bohrmann, B., Schneider, B. L., & Aebischer, P. (2016) · Brain · doi:10.1093/brain/aww036 · Cited by 49
“The mAb-11 antibody used in the present study is similar to gantenerumab, which is highly speciﬁc for amyloid plaques and reduces amyloid 1602 | BRAIN 2016: 139; 1587–1604 burden in patients with Alzheimer’s disease (Bohrmann et al. , 2012; Demattos et al. , 2012; Ostrowitzki et al. , 2012).”
Method
Characterization of the selective in vitro and in vivo binding properties of crenezumab to oligomeric Aβ
Meilandt, W. J., Maloney, J. A., Imperio, J., Lalehzadeh, G., Earr, T., Crowell, S., Bainbridge, T. W., Lu, Y., Ernst, J. A., Fuji, R. N., et al. (2019) · Alzheimer's Research & Therapy · doi:10.1186/s13195-019-0553-5 · Cited by 45
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 50
The value and limitations of transgenic mouse models used in drug discovery for Alzheimer's disease: an update
Bales, K. R. (2012) · Expert Opinion on Drug Discovery · doi:10.1517/17460441.2012.666234 · Cited by 46
“Preliminary encouraging results in small Phase II trials with bapineuzumab or gantenerumab using carbon-11-labeled PittsburghCompound B ((11)C-PIB) positron emission tomography (PET) suggest that both of these agents are affecting removal of Ab from brain [79,80].”
BackgroundResult
The Role of Antibodies and Their Receptors in Protection Against Ordered Protein Assembly in Neurodegeneration
Katsinelos, T., Tuck, B. J., Mukadam, A. S., & McEwan, W. A. (2019) · Frontiers in Immunology · doi:10.3389/fimmu.2019.01139 · Cited by 46
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
Recent advancements toward therapeutic vaccines against Alzheimer’s disease
Herline, K., Drummond, E., & Wısnıewskı, T. (2018) · Expert Review of Vaccines · doi:10.1080/14760584.2018.1500905 · Cited by 46
“The rate of ARIA-E occurred more often in APOE ε4 carriers than noncarriers and is consistent with other anti-Aβ monoclonal antibodies [68,70,71].”
Result
The application of positron emission tomography (PET) imaging in CNS drug development
Suridjan, I., Comley, R. A., & Rabiner, E. A. (2018) · Brain Imaging and Behavior · doi:10.1007/s11682-018-9967-0 · Cited by 44
A Phase I Study to Assess the Effect of Speed of Injection on Pain, Tolerability, and Pharmacokinetics After High-volume Subcutaneous Administration of Gantenerumab in Healthy Volunteers
Portron, A., Jordan, P., Draper, K., Muenzer, C., Dickerson, D., van Iersel, T. M., & Hofmann, C. (2019) · Clinical Therapeutics · doi:10.1016/j.clinthera.2019.11.015 · Cited by 43
Alzheimer’s Disease: Drug Discovery
Huang, X. (2020) · Exon Publications eBooks · doi:10.36255/exonpublications.alzheimersdisease.2020 · Cited by 49
Alzheimer Disease Pharmacologic Treatment and Treatment Research
Schneider, L. S. (2013) · CONTINUUM Lifelong Learning in Neurology · doi:10.1212/01.con.0000429180.60095.d0 · Cited by 45
Morphological and Molecular Profiling of Amyloid-β Species in Alzheimer’s Pathogenesis
Almeida, Z. L., Vaz, D. C., & Brito, R. M. M. (2024) · Molecular Neurobiology · doi:10.1007/s12035-024-04543-4 · Cited by 49
Impaired Glucose Tolerance and Reduced Plasma Insulin Precede Decreased AKT Phosphorylation and GLUT3 Translocation in the Hippocampus of Old 3xTg-AD Mice
Griffith, C. M., Macklin, L. N., Cai, Y., Sharp, A. A., Yan, X., Reagan, L. P., Strader, A. D., Rose, G. M., & Patrylo, P. R. (2019) · Journal of Alzheimer s Disease · doi:10.3233/jad-180707 · Cited by 44
“To date, no late stage (phase III) clinical trials targeting A (cid:2) [54–56] or tau [57, 58] have been successful.”
Effect of active A β immunotherapy on neurons in human Alzheimer's disease
Paquet, C., Amin, J., Mouton‐Liger, F., Nasser, M., Love, S., Gray, F., Pickering, R. M., Nicoll, J. A., Holmes, C., Hugon, J., et al. (2015) · The Journal of Pathology · doi:10.1002/path.4491 · Cited by 44
“Post mortem studies [11–13] and in vivo amyloid imaging [14,15] of patients enrolled in clinical trials confirmed that Aβ removal occurs following immunotherapy, with the extent of amyloid removal being highly variable among immunized patients, from none to nearly complete [13,16–18].”
Background
Roles of peripheral lipoproteins and cholesteryl ester transfer protein in the vascular contributions to cognitive impairment and dementia
Poliakova, T., & Wellington, C. L. (2023) · Molecular Neurodegeneration · doi:10.1186/s13024-023-00671-y · Cited by 42
“…largely via perivascular pathways and can slow cognitive decline, they are also associated with safety concerns known as amyloid related imaging abnormalities (ARIA) including edema (ARIA-E) and hemorrhage (ARIA-H) subtypes that reflect damage to cerebral vessels during amyloid clearance [33, 34].”
Background
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
Recurrence of Cerebral Amyloid Angiopathy-Related Inflammation: A Report of Two Cases from the i CAβ International Network
DiFrancesco, J. C., Touat, M., Caulo, M., Gallucci, M., Garcin, B., Lévy, R., Uncini, A., & Piazza, F. (2015) · Journal of Alzheimer s Disease · doi:10.3233/jad-150070 · Cited by 42
“This hypothesis could be supported by the evidence of transient neurological symptoms and vasogenic edema, in association with the development of MHs, and colocalized with the areas of higher A reduction at PiB-PET, in APOE 4 homozygous AD patients treated with the anti-A therapeutic antibody gantenerumab [11].”
The potential of solanezumab and gantenerumab to prevent Alzheimer’s disease in people with inherited mutations that cause its early onset
Panza, F., Seripa, D., Lozupone, M., Solfrizzi, V., Imbimbo, B. P., Barulli, M. R., Tortelli, R., Capozzo, R., Bisceglia, P., Dimitri, A., et al. (2018) · Expert Opinion on Biological Therapy · doi:10.1080/14712598.2018.1389885 · Cited by 41
Combotherapy and current concepts as well as future strategies for the treatment of Alzheimer's disease
Chiu, M., & Fan, L. (2014) · Neuropsychiatric Disease and Treatment · doi:10.2147/ndt.s45143 · Cited by 41
“Gantenerumab has been proven to reduce cerebral amyloid and is currently in Phase III studies (NCT01760005).(32) Crenezumab is another humanized antibody that targets protofibrillar epitopes of Aβ and inhibits Aβ aggregation and is currently undergoing a Phase II trial (NCT01723826).”
Background
Amyloid-β and α-Synuclein Immunotherapy: From Experimental Studies to Clinical Trials
Nimmo, J., Kelly, L., Verma, A. K., Carare, R. O., Nicoll, J. A. R., & Dodart, J. (2021) · Frontiers in Neuroscience · doi:10.3389/fnins.2021.733857 · Cited by 40
Invited review: Drug development for tauopathies
Grüninger, F. (2014) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12192 · Cited by 40
Cerebrospinal Fluid Amyloid-β 42, Total Tau and Phosphorylated Tau are Low in Patients with Normal Pressure Hydrocephalus: Analogies and Differences with Alzheimer’s Disease
Santangelo, R., Cecchetti, G., Bernasconi, M. P., Cardamone, R., Barbieri, A., Pinto, P., Passerini, G., Scomazzoni, F., Comı, G., & Magnani, G. (2017) · Journal of Alzheimer s Disease · doi:10.3233/jad-170186 · Cited by 42
“…trialsaimedatreducingbrainamyloidinADpatients byadministeringmonoclonalantibodyagainstamy-loidfailed:despitetheimagingevidencethatamyloid plaquesinthebrainsoftreatedsubjectsweresignif-icantlyreduced[97–99],thesepatientsdidnotshow anysigniﬁcantimprovementinneurocognitiveper-formances[100,101].”
Patient and carer views on participating in clinical trials for prodromal Alzheimer's disease and mild cognitive impairment
Lawrence, V. C., Pickett, J., Ballard, C. G., & Murray, J. (2013) · International Journal of Geriatric Psychiatry · doi:10.1002/gps.3958 · Cited by 39
“Several phase II trials of different antiamyloid antibodies under development have shown they can reduce Ab levels in mild to moderate Alzheimer’s disease (Rinne et al., 2010; Ostrowitzki et al., 2012; Siemers et al., 2010) and have a safety profile supporting their progression to efficacy phase III trials.”
Background
Anti-dementia medications: current prescriptions in clinical practice and new agents in progress
Stella, F., Radanovic, M., Canineu, P. R., de Paula, V. D. J. R., & Forlenza, O. V. (2015) · Therapeutic Advances in Drug Safety · doi:10.1177/2042098615592116 · Cited by 39
Immunotherapies in Alzheimer’s disease: Too much, too little, too late or off-target?
St‐Amour, I., Cicchetti, F., & Calon, F. (2015) · Acta Neuropathologica · doi:10.1007/s00401-015-1518-9 · Cited by 40
Clinical Evaluation of Amyloid-Related Imaging Abnormalities in Bapineuzumab Phase III Studies
Brashear, H. R., Ketter, N., Bogert, J., Di, J., Salloway, S., & Sperling, R. A. (2018) · Journal of Alzheimer s Disease · doi:10.3233/jad-180675 · Cited by 39
Comparative Efficacy and Safety of Monoclonal Antibodies for Cognitive Decline in Patients with Alzheimer’s Disease: A Systematic Review and Network Meta-Analysis
Qiao, Y., Gu, J., Yu, M., Chi, Y., & Ma, Y. (2024) · CNS Drugs · doi:10.1007/s40263-024-01067-2 · Cited by 38
The Use, Standardization, and Interpretation of Brain Imaging Data in Clinical Trials of Neurodegenerative Disorders
Schwarz, A. J. (2021) · Neurotherapeutics · doi:10.1007/s13311-021-01027-4 · Cited by 40
“Some imaging markers can sit in either category, with their context of use in early- or late-phase trials largely dependent on the magnitude of treatment effect— for example, the removal of amyloid plaques below baseline levels in AD can be detected in relatively small trials and represents a clear pharmacodynamic eff…”
Background
Regulation of Cerebral Cholesterol Metabolism in Alzheimer Disease
Reiss, A. B., & Voloshyna, I. (2012) · Journal of Investigative Medicine · doi:10.2310/jim.0b013e318246d973 · Cited by 38
Anti-amyloid-beta to tau-based immunization: developments in immunotherapy for Alzheimer's disease
Lambracht‐Washington, D., & Rosenberg, R. N. (2013) · ImmunoTargets and Therapy · doi:10.2147/itt.s31428 · Cited by 39
“dependent manner by up to 30%, as shown by positron emission tomography (PET) scans with the fibrillar Aβ-specific Pittsburgh B compound.(52) Another drug to treat AD with anti-Aβ antibodies,”
The neurobiology of Alzheimer disease defined by neuroimaging
Masdeu, J. C., Kreisl, W. C., & Berman, K. F. (2012) · Current Opinion in Neurology · doi:10.1097/wco.0b013e3283557b36 · Cited by 39
Aβ-Immunotherapeutic strategies: a wide range of approaches for Alzheimer's disease treatment
Montoliu‐Gaya, L., & Villegas, S. (2016) · Expert Reviews in Molecular Medicine · doi:10.1017/erm.2016.11 · Cited by 39
Targeting Beta-Amyloid at the CSF: A New Therapeutic Strategy in Alzheimer’s Disease
Menéndez‐González, M., Padilla-Zambrano, H., Alvarez, G., Capetillo‐Zarate, E., Tomás‐Zapico, C., & Costa, A. D. D. (2018) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2018.00100 · Cited by 38
“On the right, predicted evolution of Aβ levels in a case of AD treated at presymptomatic stage. islSF, insoluble pool in the ISF; slSF, soluble pool in the ISF. amyloid around the site of antibody injection (Ostrowitzki et al., 2012).”
BackgroundInfluential

Authors: Ostrowitzki, S.
Affiliations: F. Hoffmann-La Roche AG (CH)
Corresponding author: Ostrowitzki, Susanne
Venue: Archives of Neurology
Publisher: American Medical Association (AMA)
Published: 2012-02-01
Volume: 69
Issue: 2
Pages: 198
ISSN: 0003-9942 (ISSN-L)
DOI: 10.1001/archneurol.2011.1538
OpenAlex: W2118753807
Cited by: 431
References: 19
Citations by year: 2026: 18 · 2025: 17 · 2024: 34 · 2023: 22 · 2022: 22 · 2021: 24 · 2020: 18 · 2019: 23 · 2018: 30 · 2017: 34 · 2016: 39 · 2015: 31 · 2014: 44 · 2013: 45 · 2012: 24
FWCI: 25.95
Type: journal article
Language: en
Open access: closed
Locations: Archives of Neurology (publishedVersion)
PubMed (publishedVersion)
Pure Amsterdam UMC (publishedVersion)
Amsterdam UMC (VU Amsterdam) - Institutional Repository (publishedVersion)
UCL Discovery (University College London) (submittedVersion)
Data Archiving and Networked Services (DANS) (submittedVersion)
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › 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: gantenerumab, Alzheimer's disease, amyloid-beta, anti-amyloid monoclonal antibodies, phagocytosis, microglia, Pittsburgh compound B, dose-dependent effects, vasogenic edema
MeSH terms: Aged, Alzheimer Disease, Aniline Compounds, Antibodies, Monoclonal, Brain Chemistry, Cell Count, Double-Blind Method, Female, Follow-Up Studies, Humans, Immunoglobulin G, Injections, Intravenous, Male, Middle Aged, Phagocytosis, Thiazoles, Cohort Studies, Amyloid beta-Peptides, Microglia, Sample Size, Radiopharmaceuticals, Alzheimer Vaccines, Positron-Emission Tomography, Antibodies, Monoclonal, Humanized

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Mechanism of Amyloid Removal in Patients With Alzheimer Disease Treated With Gantenerumab

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