Alzheimer disease (AD) is the leading cause of dementia worldwide, and until recently, effective strategies to slow or prevent its clinical progression have been elusive. This review examines the latest advancements in biomarker technologies and therapeutic development for improving AD diagnosis and treatment. It discusses the use of neuroimaging and fluid-based biomarkers to stage AD pathology, focusing on the role of amyloid, tau, and neuroinflammation in disease progression. The review also highlights potential disease-modifying treatment targets and their implications for AD clinical care.
Alzheimer disease (AD) is the most common contributor to dementia in the world, but strategies that slow or prevent its clinical progression have largely remained elusive, until recently. This Review highlights the latest advances in biomarker technologies and therapeutic development to improve AD diagnosis and treatment. We review recent results that enable pathological staging of AD with neuroimaging and fluid-based biomarkers, with a particular emphasis on the role of amyloid, tau and neuroinflammation in disease pathogenesis. We discuss the lessons learned from randomized controlled trials, including some supporting the proposal that certain anti-amyloid antibodies slow cognitive decline during the mildly symptomatic phase of AD. In addition, we highlight evidence for newly identified therapeutic targets that may be able to modify AD pathogenesis and progression. Collectively, these recent discoveries-and the research directions that they open-have the potential to move AD clinical care toward disease-modifying treatment strategies with maximal benefits for patients. This Review summarizes recent advances in biomarkers and therapies for Alzheimer disease-the products of decades of research-and discusses the challenges, gaps and clinical implications.
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