Researchers and clinicians alike believe there is substantial evidence to support the hypothesis that Alzheimer’s disease (AD) may be caused by deposition of amyloid beta-peptide (Abeta) in plaques in brain tissue. But drugs targeted towards the beta-amyloid have met with significant setbacks challenging whether the target is, in fact, real.
With several late stage drugs targeting beta-amyloid poised for market entry, a panel of opinion leaders in the treatment of Alzheimer’s and scientific industry specialists discussed the issue at the 2012 BIO CEO & Investor Conference.
Joshua Schimmer, managing director of biotechnology for Leerink Swann, moderated a panel that included:
- Ted T. Ashburn, MD, PhD, Project Head, Leukine® (sargramostim) and Elitek®/Fasturtec® (rasburicase), Sanofi Oncology
- Michael Gold, MS, MD, Vice President, Clinical Development & Chief Medical Officer, Allon Therapeutics Inc.
- Marc L. Gordon MD, Chief of Neurology, Associate Professor of Neurology and Psychiatry, Zucker Hillside Hospital, Hofstra North Shore-LIJ School of Medicine
- Hyoung-Gon Lee, PhD, Assistant Professor, Pathology and Neurology, Case Western Reserve University School of Medicine
With all the questions surrounding the beta-amyloid process, Schimmer asked the panelists: “Why don’t we spend billions of dollars to figure out what ABP is doing?”
“It very well could be that this is the wrong target to be going after,” Ashburn replied. “I think with these [recent] failures there are really three things to think about. Is it target problem? Is it a compound problem? Or, is it a methodological problem?”
However, the panelists did agree that it’s very likely that amyloid has something to do with Alzheimer’s disease – it’s just a question of degree.
“Hopefully, in the not too distant future, we have drugs that can do something,” Ashburn said. “The doctor will hopefully have a repertoire of mechanisms to bring to bear as he or she does today with hypertension.”