¹⁸F–THK–5351, Fluorodeoxyglucose, and Florbetaben PET Images in Atypical Alzheimer’s Disease: A Pictorial Insight into Disease Pathophysiology

• Main Authors: Sohee Park, Minyoung Oh, Jae Seung Kim, Jae-Hong Lee, Young Wook Yoon, Jee-Hoon Roh
• Format: Article
• Language: English
• Published: MDPI AG 2021-04-01
• Series: Brain Sciences
• Subjects: ¹⁸F–THK–5351 PET; atypical Alzheimer’s disease (AD); posterior cortical atrophy (PCA); logopenic variant of primary progressive aphasia (lpvPPA)
• Online Access: https://www.mdpi.com/2076-3425/11/4/465

The recent advance of positron emission tomography (PET) tracers as biomarkers in Alzheimer’s disease (AD) provides more insight into pathophysiology, preclinical diagnosis, and further therapeutic strategies. However, synergistic processes or interactions between amyloid and tau deposits are still poorly understood. To better understand their relationship in focal brain changes with clinical phenotypes, we focused on region-specific or atypical AD characterized by focal clinical presentations: Posterior cortical atrophy (PCA) and logopenic variant of primary progressive aphasia (lpvPPA). We compared three different PET images with ¹⁸F–THK–5351 (tau), ¹⁸F–Florbetaben (amyloid beta, Aβ), and ¹⁸F–Fluorodeoxyglucose (glucose metabolism) to investigate potential interactions among pathologies and clinical findings. Whereas the amyloid accumulations were widespread throughout the neocortex, tau retentions and glucose hypometabolism showed focal changes corresponding to the clinical features. The distinctly localized patterns were more prominent in tau PET imaging. These findings suggest that tau pathology correlates more closely to the clinical symptoms and the neurodegenerative processes than Aβ pathology in AD.