Integrating amyloid and tau imaging with proteomics and genomics in Alzheimer’s disease

Abstract

Alzheimer’s disease (AD) is the most common neurodegenerative disease and is characterized by the aggregation of β-amyloid (Aβ) and tau in the brain. Breakthroughs in disease-modifying treatments targeting Aβ bring new hope for the management of AD. But to effectively modify and someday even prevent AD, a better understanding is needed of the biological mechanisms that underlie and link Aβ and tau in AD. Developments of high-throughput omics, including genomics, proteomics, and transcriptomics, together with molecular imaging of Aβ and tau with positron emission tomography (PET), allow us to discover and understand the biological pathways that regulate the aggregation and spread of Aβ and tau in living humans. The field of integrated omics and PET studies of Aβ and tau in AD is growing rapidly. We here provide an update of this field, both in terms of biological insights and in terms of future clinical implications of integrated omics-molecular imaging studies.