Bevacizumab treatment for human glioblastoma. Can it induce cognitive impairment?

• Published in: Neuro-oncology (Charlottesville, Va.) Va.), 2014-05, Vol.16 (5), p.754-756
• Main Authors: Fathpour, Pakzad, Obad, Nina, Espedal, Heidi, Stieber, Daniel, Keunen, Olivier, Sakariassen, Per Ø, Niclou, Simone P, Bjerkvig, Rolf
• Format: Article
• Language: English
• Subjects: Angiogenesis Inhibitors - adverse effects; Angiogenesis Inhibitors - pharmacology; Animals; Antibodies, Monoclonal, Humanized - adverse effects; Antibodies, Monoclonal, Humanized - pharmacology; Bevacizumab; Brain Neoplasms - drug therapy; Cognition Disorders - chemically induced; Glioblastoma - drug therapy; Hippocampus - drug effects; Humans; Letters to the Editor; Neuronal Plasticity - drug effects; Rats
• ISSN: 1522-8517; 1523-5866
• DOI: 10.1093/neuonc/nou013

Recent results from 2 double-blind, placebo-controlled phase III trials (RTOG 0825) and (AVAglio) for first-line treatment of glioblastoma patients with the VEGF antibody bevacizumab, showed similar results, related to overall and progression-free survival. The RTOG 0825 trial indicated, opposed to the AVAglio trial, that patients treated with bevacizumab showed a decline in global neurocognitive function compared to untreated patients, -a decline that was most obvious after prolonged treatment. At present, there is a considerably controversy related to these observations. In the present work we point at the possibility that bevacizumab treatment of the normal brain can reduce synaptic plasticity in the hippocampus. We believe that such a phenomenon may partly explain the reduced cognitive function observed in patients in the RTOG 0825 trial. Since the same effects were not clearly defined in the AVAglio trial, further studies on putative neurocognitive effects after bevacizumab treatment are warranted.