Industry Focuses on Earlier Intervention in Alzheimer's
Today the WSJ provides a very high-level overview of the currently prevailing idea for meaningful Alzheimer's treatment: attack earlier. The conclusion is largely based on increasingly disappointing results of anti-amyloid drugs in development (from Pfizer/JNJ, Lilly, and BMS), which have been tested in established disease.
Some scientists speculate (and it's all speculation) that amyloid deposition in the brain may be most toxic before symptoms of clinical dementia appear, the WSJ notes. Others imply that follow-up tau-related deposits are the major instigator of brain damage. The WSJ cites one study, presented at the recent ICAD conference, in which there was little change in amyloid deposits among patients "progressing toward Alzheimer's" but "substantial changes in tau and brain volumes."
The quoted industry cheerleaders, who (understandably) remain tireless in their efforts to find uses for their companies' investigational anti-amyloid agents:
Howard Feldman, MD, BMS's vice president of global clinical research for neuroscience ("Earlier intervention will allow us to treat patients when they have much less disability and when it could still be possible to prevent or delay such [memory] losses");
Rachel Schindler, MD, Pfizer's executive director for Alzheimer's disease ("The growing evidence from biomarkers has led to a greater acceptance in the field of looking towards earlier treatment"); and
Eric Siemers, MD (right), senior medical director for Alzheimer's disease ("There's not quite a template,but there's a broad acknowledgment of how important [linking biomarkers to disease progression] is"). The Midwesterner—to his credit—has a very accessible, almost mild-mannered way of speaking, which is probably keeping some Lilly shareholders from running for the hills.
Some scientists speculate (and it's all speculation) that amyloid deposition in the brain may be most toxic before symptoms of clinical dementia appear, the WSJ notes. Others imply that follow-up tau-related deposits are the major instigator of brain damage. The WSJ cites one study, presented at the recent ICAD conference, in which there was little change in amyloid deposits among patients "progressing toward Alzheimer's" but "substantial changes in tau and brain volumes."
The quoted industry cheerleaders, who (understandably) remain tireless in their efforts to find uses for their companies' investigational anti-amyloid agents:
Howard Feldman, MD, BMS's vice president of global clinical research for neuroscience ("Earlier intervention will allow us to treat patients when they have much less disability and when it could still be possible to prevent or delay such [memory] losses");
Rachel Schindler, MD, Pfizer's executive director for Alzheimer's disease ("The growing evidence from biomarkers has led to a greater acceptance in the field of looking towards earlier treatment"); and
Eric Siemers, MD (right), senior medical director for Alzheimer's disease ("There's not quite a template,but there's a broad acknowledgment of how important [linking biomarkers to disease progression] is"). The Midwesterner—to his credit—has a very accessible, almost mild-mannered way of speaking, which is probably keeping some Lilly shareholders from running for the hills.
