AC Immune reports initial interim data from Phase 1b trial of ACI-24 vaccine
AC Immune announced initial interim data from an ongoing Phase 1b trial of the ACI-24 anti-Abeta vaccine to treat Alzheimer's disease like symptoms in subjects with Down syndrome as well as key takeaways from its Key Opinion Leader meeting, held in New York City. The event is being co-chaired by Professor Pfeifer and Professor William Mobley, Executive Director of the University of California San Diego's Down Syndrome Center for Research and Treatment. It features presentations from Professor Mobley and Dr. Brian Skotko, Associate Professor at Harvard Medical School and the Emma Campbell Endowed Chair on Down Syndrome and Director of the Down Syndrome Program at Massachusetts General Hospital, as well as Professor Pfeifer and Dr. Marie Kosco-Vilbois, Chief Scientific Officer of AC Immune. Highlights of Dr. Skotko's presentation include: DS is caused by having a third copy of chromosome 21 and occurs in 1/~792 live births; ~5,000 children per year, ~212,000 people living with DS in the US and ~359,000 in Europe; Adults with DS are increasingly moving into semi-independent living situations and securing paid employment, are involved in romantic relationships and marry, participate in day habilitation services or are active participants in sports. Initial symptoms are typically changes in behavior; seizures can also be an early warning sign, followed by memory loss Based on surveys, family members and people with DS say they are satisfied, even positive, about their lives despite acknowledging the challenges that accompany DS. Highlights from Professor Mobley's presentation include: The neuropathological changes in DS subjects are very similar but not identical to typical AD. People with Down syndrome have an extra copy of chromosome 21, which houses the gene that codes for amyloid precursor protein. APP is the parent protein of Abeta, a protein fragment that accumulates into amyloid plaques, a key feature of AD; Studying AD-like symptoms in the DS population addresses many of the key dilemmas that hinder the discovery of new treatments: uncertain mechanisms and timing of disease-induced brain changes, difficulty offering treatment before disease onset, genetic and age-related variability, and the risk of including subjects with other forms of age-related dementia; For AD in DS, the disease mechanism and approximate timing of onset are known; readily detectable pathological changes occur prior to AD-like symptoms, enabling treatment prior to disease onset; the DS population is far more homogeneous and carries minimal risk of having coexisting conditions causing dementia at such a young age; In mouse models of DS, vaccination against Abeta by ACI-24 improved cognition and prevented neuronal atrophy.