Pathophysiology of Alzheimer’s disease revealed by chemical exchange saturation transfer MRI

Abstract

Alzheimer’s disease (AD) is the most common neurodegenerative brain disorder that is characterized by the deposition of amyloid-β protein (Aβ) and neurofibrillary aggregates (tau). There is currently no cure for AD; however, early diagnosis and intervention may prevent progression to dementia. In addition to CSF and blood biomarkers, imaging techniques, such as PET, fMRI, volumetric MRI, and chemical exchange saturation transfer (CEST), have facilitated the early diagnosis of AD and provided essential information about the pathophysiology of AD. Indeed, CEST findings have helped clarify important aspects of the pathophysiology underlying AD. In this article we provide an in-depth review of different CEST applications, including endogenous CEST (APT, creatine-CEST, and glutamate-CEST) and exogenous CEST (angiopep2, glucose, and glymphatic system-related CEST), in further elucidating the pathophysiology of AD and discuss the potential of novel approaches.