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Combined treatment with a BACE inhibitor and anti-abeta antibody gantenerumab enhances amyloid reduction in APP London mice

Bibliographic

Year of Publication:
2014
Contact PI Name:
Bernd Bohrmann
Contact PI Affiliation:
Pharma Research BS Early Development, DTA Neuroscience, Basel, Switzerland
Co-Authors:
Helmut Jacobsen, Laurence Ozmen, Antonello Caruso, Robert Narquizian, Hans Hilpert, Bjoern Jacobsen, Dick Terwel, An Tanghe
Primary Reference (PubMED ID):
Funding Source:
Not Reported
Study Goal and Principal Findings:

The goal of this study was to evaluate the beta amyloid lowering effects of a combined intervention of a BACE1 inhibitor and beta amyloid specific antibody,speciifically to comapre the efficacy of the combination to that of the individual therapeutic agents. To this end investigators performed a chronic study in APPLondon transgenic mice that received treatment with anti-Aβ antibody gantenerumab and BACE inhibitor RO5508887, either as mono- or combination treatment. Mono-treatments with either compound caused a dose-dependent reduction of total brain Aβ and amyloid burden.Mono therapy using the BACE inhibitor significantly reduced the amounts of total brain Aβ40 and Aβ42 compared with the vehicle group, with a clear dose-dependency. Gantenerumab alone significantly reduced the amount of  brain Aβ42 species by 39%, whereas no significant decrease was observed for Aβ40. Combination treatment with both compounds significantly enhanced the anti-amyloid effect as measured by total brain Aβ40 and Aβ42.  The decrease of Aβ42 in the combination treatment was 66% compared with 28% with BACE inhibitor alone, a clear doubling of efficacy. The effect is additive, because the reduction with antibody alone was 39%. The effect of the combination on Aβ40 as much less pronounced.The observed combination effect was most pronounced for lowering of amyloid plaque load and plaque number, which suggests effective inhibition of de novo plaque formation. Moreover, significantly enhanced clearance of pre-existing amyloid plaques was observed with the combination therapy compared to the mono-therapies. In addition BACE inhibition by RO5508887  led to a significant time- and dose-dependent decrease in CSF Aβ, which was not observed for gantenerumab treatment. These results demonstrate that combining these two anti-amyloid agents enhances overall efficacy and suggests that combination treatments may be of clinical relevance.

Bibliographic Notes:
Helmut Jacobsen and Bernd Bohrmann ( Pharma Research BS Early Development, DTA Neuroscience, Basel, Switzerland) are corresponding authors on this paper.

Therapeutic Agent

Therapeutic Information:
Therapy Type:
Small Molecule
Therapeutic Agent:
RO5508887
Therapeutic Target:
BACE1
Therapy Type:
Biologic - Immunotherapy(passive)
Therapeutic Agent:
Gantenerumab
Therapeutic Target:
beta Amyloid Peptide

Animal Model

Model Information:
Species:
Mouse
Model Type:
APP
Strain/Genetic Background:
(C57BL/6.FVB/N)

Experimental Design

Is the following information reported in the study?:
Power/Sample Size Calculation
Randomized into Groups
Blinded for Treatment
Blinded for Outcome Measures
Pharmacokinetic Measures
Pharmacodynamic Measures
Toxicology Measures
ADME Measures
Biomarkers
Dose
Formulation
Route of Delivery
Duration of Treatment
Frequency of Administration
Age of Animal at the Beginning of Treatment
Age of Animal at the End of Treatment
Sex as a Biological Variable
Study Balanced for Sex as a Biological Variable
Number of Premature Deaths
Number of Excluded Animals
Statistical Plan
Genetic Background
Inclusion/Exclusion Criteria Included
Conflict of Interest

Outcomes

Outcome Measured
Outcome Parameters
Histopathology
beta Amyloid Load
beta Amyloid Deposits
Biochemical
Brain-beta Amyloid Peptide 40
Brain-beta Amyloid Peptide 42
CSF-beta Amyloid Peptide 40
CSF-beta Amyloid Peptide 42
Biomarker
CSF-beta Amyloid Peptide 40
CSF-beta Amyloid Peptide 42
Pharmacodynamics
Target Engagement (Reduction beta Amyloid Peptide 40-CSF)
Target Engagement (Reduction beta Amyloid Peptide 42-CSF)
Target Engagement (Reduction beta Amyloid Peptide 40-Brain)
Target Engagement (Reduction beta Amyloid Peptide 42-Brain)