These families help researchers find Alzheimer's treatments. Their network is at risk

The Dominantly Inherited Alzheimer Network (DIAN), an international research group of over 200 families across 18 countries, relies on participants carrying gene mutations that guarantee early-onset Alzheimer’s. These families, like June Ward, a 64-year-old with a high-risk mutation, volunteer for studies to help future generations avoid the disease. DIAN, led by WashU Medicine in St. Louis, has been pivotal in advancing Alzheimer’s research, including identifying a 20-year pre-symptomatic brain change period and proving early amyloid reduction can delay symptoms. Founded in 2008 with NIH funding, DIAN created the first global registry for families with rare mutations causing Alzheimer’s in their 40s or 50s. Each child of a carrier has a 50% chance of inheriting the mutation, making these families uniquely valuable for predicting disease onset. Studies like DIAN-TU, launched in 2012 with the Alzheimer’s Association and pharmaceutical partners, demonstrated that drugs targeting amyloid plaques could slow progression. A 2025 study showed early intervention could delay symptoms in mutation carriers. DIAN’s discoveries also revealed rare cases where individuals with high-risk mutations never develop Alzheimer’s, offering potential clues for protective mechanisms. The network’s trials directly contributed to the approval of lecanemab and donanemab, two amyloid-targeting drugs now on the market. However, DIAN’s future is uncertain due to federal funding cuts and delays from the National Institutes of Health (NIH). Without continued support, the network’s infrastructure, trained participants, and long-term relationships could dissolve, jeopardizing years of progress. Dr. Tammie Benzinger, who oversees brain imaging for DIAN, warned that funding gaps would dismantle the network’s carefully built foundation. Dr. Randall Bateman, co-director of DIAN and a neurology professor at WashU Medicine, emphasized the families’ role in answering critical questions about Alzheimer’s onset. The rare mutations, though few in number, provided the only population where researchers could predict both *who* would develop the disease and *when*. Without DIAN, Bateman noted, key advancements in early detection and treatment might never have been possible. The NIH’s pending grant decisions will determine whether DIAN can continue essential functions, including clinical trials and participant monitoring. Families like Ward’s, who participate despite knowing they may never benefit personally, remain committed to the cause. Their legacy could shape Alzheimer’s treatment for generations—but only if funding stabilizes. The network’s survival hinges on securing long-term financial backing to sustain its groundbreaking work.