Alzheimer’s disease is the most common form of dementia among older people. Misfolding
and aggregation of proteins (amyloid-β and tau) in the brain is the primary cause of neurodegeneration
in the disease. Non-invasive detection of amyloid-β deposition can be realized using positron emission
tomography probes, but a proportion of Aβ-positive subjects do not present with cognitive dysfunction,
suggesting limitations in assessment using this method. Non-invasive detection of tau deposits in the
brain can be used to diagnose, monitor, and predict Alzheimer’s disease progression. Tau positron
emission tomography radiolabelled probes such as T807, THK-5117, and PBB3 can image the pathology
of the disease in vivo. The 18F-labeled tau imaging agents 18F-THK-5351, 18F-T807 (18F-AV-1451),
and 18F-RO6958948 are presently under evaluation in clinical studies and clinical trials worldwide.
This imaging methodology could be applied to enable preclinical diagnoses and disease-modifying
drugs for Alzheimer’s disease. In this review, we provide an overview of the pathology and potential
imaging of tau in Alzheimer’s disease, development of a THK series among tau tracers, and the chemical,
radiochemical, biological, and clinical features of tau probes.
Keywords: Alzheimer’s disease, aggregation, brain, amyloid-β, tau, positron emission tomography, THK series, protein.
Rights & PermissionsPrintExport