The LEARN Project will Track Cognitive Change in a Comparison Group of Older Individuals, and Initiate the First Tau Imaging Study in a Longitudinal Prevention Trial
The Alzheimer’s Association today announced its largest ever research grant — $8 million over four years — to support the Longitudinal Evaluation of Amyloid Risk and Neurodegeneration (LEARN) study as a companion study to the Anti-Amyloid Treatment in Asymptomatic Alzheimer’s Disease (A4) Study, a pioneering Alzheimer’s prevention trial that is starting this year.
The grant was awarded to Reisa Sperling, M.D., M.M.Sc., professor of neurology at Harvard Medical School, director of the Center for Alzheimer Research and Treatment at Brigham and Women’s Hospital and Massachusetts General Hospital, and co-principal investigator of the A4 Trial.
A first of its kind study, one objective of LEARN is to determine causes of cognitive decline besides buildup of an abnormal protein called amyloid beta in the brain. Amyloid beta “plaques” are a hallmark brain lesion of Alzheimer’s discernable during life by specialized PET imaging, and also at autopsy. To that end, a subset of study participants will have an innovative PET scan of the brain for buildup of tau protein, which makes up neurofibrillary tangles, the other hallmark Alzheimer’s brain lesion.
LEARN was developed in complement to the A4 Study, which is investigating whether treatments that block amyloid beta protein build up in the brain can slow or prevent Alzheimer’s in those people who do not yet have memory and thinking problems. A4 is unique because it will specifically look at individuals who are cognitively normal and have no known Alzheimer’s-related genetic mutations, but are thought to be at risk to develop the disease because of buildup of the amyloid beta protein in their brains. A4 will test if giving this population an anti-amyloid treatment will not only change this amyloid buildup, but more importantly slow or prevent Alzheimer’s disease.
The LEARN subcomponent of A4 will follow over time individuals who do not have elevated amyloid and determine what biological changes are related to cognitive decline, including possible later amyloid buildup as well as increases in tau levels and a variety of other measures, helping to shed light on the perplexing individual variation in disease progression.
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