Type:
Educational Exhibit
Keywords:
Dementia, Radiobiology, PET, Nuclear medicine, Neuroradiology brain, Molecular imaging
Authors:
A. Bhandari, K. Jang, M. Sathi, J. O'Sullivan, P. Nestor; QLD/AU
DOI:
10.26044/ranzcr2019/R-0100
Background
With the development of newer tau specific radiotracers there is interest in whether 4 repeat (4R) predominant taupathies—progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD) and its clinical syndrome, corticobasal syndrome—can be differentiated from idiopathic Parkinson’s disease (IPD) and multiple system atrophy (MSA) that are α-synucleinopathies.1 This has clinical implications as treatment differs – for example atypical parkinsonian disorders (CBS, PSP and MSA) do not respond to levodopa to the same magnitude as IPD.2 Studies correlating clinical features with pathological diagnosis have shown that clinical diagnosis can be problematic in these disorders.3 Clinical diagnosis in many cases does not correlate with the gold standard of diagnosis on autopsy.4 Functional imaging of tau proteins may provide a means of diagnosing and differentiating between these parkinsonian disorders.