The trial involves 300 Colombian volunteers: 100 of whom are Paisa mutation carriers given a drug, 100 are Paisa mutation carriers given a placebo, and 100 are non-carriers given a placebo. The promising drug, crenezumab, clears the brain of amyloid plaques which cause AD. Unaware of whether they carry and are being treated for the mutation, volunteers are injected with the drug every two weeks for five years and monitored with memory tests and brain scans– results arrive in 2021.4
Free from complications of old age, these young Colombians with Alzheimer's have “cleaner brains that can give a better picture” of whether drugs work, even in cases of non-familial, late-onset AD (Buckholtz). Not to mention their participation allows researchers like Dr. John C. Morris of Washington University in St. Louis to devise an attack before the disease develops: “The brain is badly damaged by the time (carriers) have dementia...perhaps the reason our therapies have been ineffective or mostly ineffective is that we’re administering them too late,” Morris contemplates.
Such preventive research examines early changes in E280A carriers that precede symptoms, or “biomarkers,” An offshoot of the Lopera’s $100M study found a notable difference between carriers and non-carriers as young as nine years old. Those of Colombian kindred, paisa mutation carriers, “push” the circuitry surrounding the hippocampus harder to perform as well as their non-carrier peers. Moreover, young mutation carriers carry the APOE4 allele, a variation of the APOE genotype suspected to determine the age of onset.2 Whether or not these observations are significant, the study is invaluable to Colombian people at the highest imminent risk of Alzheimer’s for its access to treatment they wouldn’t otherwise have.
Among Colombian countrymen, the paisa mutation is synonymous to the mental destruction of loved ones, but from tragedy emerges hope. The isolated state of Antioquia, where Alzheimer's afflicts the young adults of each generation, is now central to the discussion of neurodegenerative disease. Ongoing studies of the early-onset Alzheimer’s phenomenon can provide clues for the preventive treatment of common Alzheimer's, quell the projected rate of Alzheimer's in 2050, and provide relief to affected families. “Prevent even one early-onset patient from getting the disease, that’s a major victory.”