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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“However, two patients in the 200 mg group showed vasogenic edema and focal areas of inflammation on MRI scans at sites with the highest level of amyloid removal (84).”
Background
Disease Modeling and Model‐Based Meta‐Analyses to Define a New Direction for a Phase III Program of Gantenerumab in Alzheimer’s Disease
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“However, higher doses of anti- amyloid antibodies were associated with more ARIA events, as shown by the PRIME study(10) and our multiple ascending dose trial (NCT00531804).(7) Therefore, the clinical benefits of a dose increase must be weighed against the increased risk of ARIA.”
BackgroundMethodResultInfluential
Immunotherapeutic approaches for Alzheimer’s disease: Exploring active and passive vaccine progress
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“Gantenerumab has been proven to reduce cerebral amyloid [98], and an RCT is currently underway to evaluate effects on cognition, function, and the safety and pharmacokinetics in patients with prodromal AD (DIAN study) alongside solanezumab [99].”
Background
Effects of an Aβ-antibody fragment on Aβ aggregation and astrocytic uptake are modulated by apolipoprotein E and J mimetic peptides
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Immunotherapy for the treatment of Alzheimer's disease: amyloid-β or tau, which is the right target?
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“Furthermore, treatment given to AD patients who were Apoε4 carriers resulted in reversible vasogenic edema.(72) A Phase III clinical trial is now”
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Immunotherapy in Alzheimer’s Disease: Current Status and Future Directions
Vashisth, K., Sharma, S., Ghosh, S., Babu, M. A., Ghosh, S., Iqbal, D., Kamal, M., Almutary, A. G., Jha, S. K., Ojha, S. K., et al. (2024) · Journal of Alzheimer s Disease · doi:10.3233/jad-230603 · Cited by 13
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PET/CT/MRI in Clinical Trials of Alzheimer’s Disease
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“6) [106, 107] but to a low degree in ARIA [108].”
Amyloid solutions: lecanemab, gantenerumab, and donanemab in the treatment of Alzheimer's disease
Ameen, T. B., Ali, U., Salma, O., Samee, M. A., Abbas, S. M. I., Kashif, S. N., Arifi, M. A., Ali, M., Khowaja, M., Ali, S. M. S., et al. (2025) · The Egyptian Journal of Neurology Psychiatry and Neurosurgery · doi:10.1186/s41983-025-00968-3 · Cited by 20
“…[146] Phase 1: 40–50% plaque reduction [203, 206]; Phase 2: 67.8% clearance [207] Dose-dependent plaque reduction; subtherapeutic early dosing [218, 226] ARIA incidence ARIA-E < 10% [143, 144]; higher in ApoE4 [148, 149] ARIA-E 6.1% (Phase II) [207, 208]; 24% (Phase III) [209, 210] ARIA-E 10%…”
Influential
The antigen-binding fragment of human gamma immunoglobulin prevents amyloid β-peptide folding into β-sheet to form oligomers
Valls-Comamala, V., Guivernau, B., Bonet, J., Puig, M., Perálvarez‐Marín, A., Palomer, E., Fernàndez‐Busquets, X., Altafaj, X., Tajes, M., Puig‐Pijoan, A., et al. (2017) · Oncotarget · doi:10.18632/oncotarget.17074 · Cited by 13
“Although none of them has overcome phase III for mild to moderate AD until now [30, 31], some trials are still ongoing because of their potential [32, 34, 35].”
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Could immunomodulation be used to prevent prion diseases?
Wısnıewskı, T., & Goñi, F. (2012) · Expert Review of Anti-infective Therapy · doi:10.1586/eri.11.177 · Cited by 13
Clinical trials in Alzheimer's disease
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Application of mesenchymal stem cells for neurodegenerative diseases therapy discovery
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ALZHEIMER’S DISEASE: DIAGNOSIS AND TREATMENT
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Roles of Microglia in AD Pathology
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Correlations between Alzheimer’s Disease Cerebrospinal Fluid Biomarkers and Cerebral Glucose Metabolism after 12 Months of Phenserine Treatment
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A Tau-Driven Adverse Outcome Pathway Blueprint Toward Memory Loss in Sporadic (Late-Onset) Alzheimer’s Disease with Plausible Molecular Initiating Event Plug-Ins for Environmental Neurotoxicants
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“Immunotherapies directed at Aβ in AD patients can be effective in decreasing Aβ deposition in the brain, but it has not led to an improvement in clinical symptoms or decreased accumulation of Tau (Ostrowitzki et al., 2012; Doody et al., 2014; Salloway et al., 2014).”
Background

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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