Effect of immunotherapy with bapineuzumab on cerebrospinal fluid biomarker levels in patients with mild to moderate Alzheimer disease

Arch Neurol. 2012 Aug;69(8):1002-10. doi: 10.1001/archneurol.2012.90.

Abstract

Background: Given the slow and variable clinical course of Alzheimer disease, very large and extended clinical trials are needed to identify a beneficial clinical effect of disease-modifying treatments. Therefore, biomarkers are essential to prove that an anti-β-amyloid (Aβ) drug candidate affects both Aβ metabolism and plaque load as well as downstream pathogenic mechanisms.

Objective: To evaluate the effect of the anti-Aβ monoclonal antibody bapineuzumab on cerebrospinal fluid (CSF) biomarkers reflecting Aβ homeostasis, neuronal degeneration, and tau-related pathology in patients with Alzheimer disease.

Design: Two phase 2, multicenter, randomized, double-blind, placebo-controlled clinical trials of 12-month duration.

Setting: Academic centers in the United States (Study 201) and England and Finland (Study 202).

Patients: Forty-six patients with mild to moderate Alzheimer disease.

Interventions: Patients received either placebo (n = 19) or bapineuzumab (n = 27) in 3 or 4 ascending dose groups.

Main outcome measures: Changes between end of study and baseline in the exploratory CSF biomarkers Aβ1-42, AβX-42, AβX-40; total tau (T-tau); and phosphorylated tau (P-tau).

Results: Within the bapineuzumab group, a decrease at end of study compared with baseline was found both for CSF T-tau (-72.3 pg/mL) and P-tau (-9.9 pg/mL). When comparing the treatment and placebo groups, this difference was statistically significant for P-tau (P = .03), while a similar trend for a decrease was found for T-tau (P = .09). No clear-cut differences were observed for CSF Aβ.

Conclusions: To our knowledge, this study is the first to show that passive Aβ immunotherapy with bapineuzumab results in decreases in CSF T-tau and P-tau, which may indicate downstream effects on the degenerative process. Cerebrospinal fluid biomarkers may be useful to monitor the effects of novel disease-modifying anti-Aβ drugs in clinical trials. TRIAL REGISTRATIONS clinicaltrials.gov Identifier: NCT00112073, EudraCT Identifier: 2004-004120-12, and isrctn.org Identifier: ISRCTN17517446.

Publication types

  • Clinical Trial, Phase II
  • Multicenter Study
  • Randomized Controlled Trial
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Alzheimer Disease / cerebrospinal fluid*
  • Alzheimer Disease / drug therapy*
  • Alzheimer Disease / epidemiology
  • Amyloid beta-Peptides / cerebrospinal fluid
  • Antibodies, Monoclonal, Humanized / therapeutic use*
  • Biomarkers / cerebrospinal fluid
  • Cohort Studies
  • Double-Blind Method
  • England / epidemiology
  • Female
  • Finland / epidemiology
  • Humans
  • Immunotherapy / methods
  • Male
  • Middle Aged
  • Peptide Fragments / cerebrospinal fluid
  • Treatment Outcome
  • United States / epidemiology
  • tau Proteins / cerebrospinal fluid

Substances

  • Amyloid beta-Peptides
  • Antibodies, Monoclonal, Humanized
  • Biomarkers
  • Peptide Fragments
  • amyloid beta-protein (1-42)
  • tau Proteins
  • bapineuzumab

Associated data

  • ClinicalTrials.gov/NCT00112073
  • ISRCTN/ISRCTN17517446