New drug, deployed early, could slowdown Alzheimer's disease

Posted Feb 7, 2020 by Tim Sandle
Could a drug deployed at the earliest hint of Alzheimer's stop or slow the disease? This appears to be a possibility based on a hypothesis put forward by the Keck School of Medicine, ahead of a planned clinical trial.
A woman suffering from Alzheimer s disease
A woman suffering from Alzheimer's disease
Philippe Huguen, AFP/File
Keck School of Medicine is based at the University of Southern California (USC) and one of its research groups, Kecks Alzheimer’s Therapeutic Research Institute (ATRI), is about to commence a major clinical study to determine if a medication coded BAN2401 has the ability to clear or prevent the buildup of amyloid plaques in the brain.
Amyloid plaques are clumps of beta-amyloids, which destroy connections between nerve cells. Since they are found in the brains of patients with Alzheimer's disease, there is a medical consensus that this build-up is connected to the development of the neureodegenerative condition.
The aim of the study is to assess whether a recombinant antibody has the potential to slow or even to stop the progression of Alzheimer’s disease by targeting plaques during the earliest stages of the illness.
The AHEAD 3-45 Study is supported by the National Institute on Aging together with the Japanese medical company Eisai Inc.
Commenting on the research plan, Laura Mosqueda from USC says: "Alzheimer’s disease is an urgent problem, with almost 6 million Americans plus their loved ones affected by this illness,” adding that “ATRI’s expertise in clinical trial design and implementation and data analysis, along with a strong commitment to sharing data to advance the field, makes me confident USC will make significant progress in identifying a treatment for this terrible disease.”
The novel BAN2401 medicine has been designed to bind to amyloid, and it is administered by intravenous injection. By connecting with beta amyloid the aim is to neutralize the protein and also to “tag” it, so that the body's immune system can recognize it and clear it from the brain.
BAN2401 is the humanized IgG1 version of the mouse monoclonal antibody mAb158, which selectively binds to large, soluble beta-amyloids protofibrils. The study to measure how effective this is will run for four-years and it will involve some 9,000 patients.