Tau Imaging in Parkinsonism: What Have We Learned So Far?

Background Positron emission tomography ligands are now available that bind to tau proteins in the brain, providing the exciting opportunity to assess the presence and distribution of tau in vivo in living patients. Methods This manuscript performed a systematic review of studies that have performed tau PET imaging in patients with parkinsonian disorders. PubMed was searched through November 13, 2017 and the review included case reports and patient‐control studies. Results Most tau‐ PET studies have utilized the [ 18 F] AV ‐1451 ligand, with a few using the [ 11 C] PBB 3 and [ 18 F] THK ‐5351 ligands. Elevated cortical tau‐ PET uptake has been observed in Parkinson's disease dementia and dementia with Lewy bodies, presumed to be related to Alzheimer's disease‐related pathology. Mild patterns of tau‐ PET uptake have been observed in subcortical structures in progressive supranuclear palsy and subcortical structures and motor cortex in corticobasal syndrome, although discrepancy with autoradiographic studies that show lack of binding to 4‐repeat tau and “off‐target” binding observed in subcortical structures limit the interpretation of these findings. Findings in frontotemporal dementia with tau mutations are variable, but elevated signal is most pronounced in mutations with deposition of both 3 and 4‐repeat tau. Elevated tau‐ PET uptake has also been observed in multiple system atrophy, a synucleinopathy. Conclusion The value of the current generation of tau‐ PET ligands varies across parkinsonian syndromes, depending upon underlying variability in tau pathology and “off‐target” binding. More work is needed to understand the biological basis of binding and more specific tau PET ligands are needed to study parkinsonian disorders.