Abstract
OPINION article Front. Neurol., 09 March 2015Sec. Brain Imaging Methods https://doi.org/10.3389/fneur.2015.00038
Highlights
F-18 FDDNP demonstrates binding to both β-amyloid and tau pathology. Another tau-targeting radiotracer, THK-523, had an uptake pattern in Alzheimer’s disease (AD) patients that was not distinguishable from healthy controls [12]. Preliminary data for another agent from this group, F-18 TKH5105, an arylquinoline derivative, have shown that this probe selectively binds to pathological paired helical filaments (PHFs) taudeposition in living patients with AD, and may differentiate diseased brains from healthy controls
18F-AV-1451 [(F-18)T807] is in Phase 2 development as a diagnostic positron emission tomography (PET) tracer for in vivo imaging of tau aggregate pathology in patients with AD and related neurodegenerative diseases characterized by the presence of tau pathology (Figure 1)
The results suggested that 18F-AV-1451 selectively bound to PHFs, and has very weak or no affinity to the β-amyloid accumulation: an approximately 29 times greater difference was found between binding to tau aggregates compared to βamyloid in the gray matter of AD brains [14]
Summary
PET imaging of tau pathology in Alzheimer’s disease and tauopathies The ability to identify and evaluate the severity of tau pathology in the brain may further assist affirmative diagnosis of AD and disease progression staging (possibly even after β-amyloid deposition plateaus)and offer evaluation of potential anti-tau treatment efficacy.
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