Sintini et al investigated whether baseline and longitudinal patterns of tau-PET uptake and MRI grey matter volume loss mirror clinical phenotype in Alzheimer’s disease. Participants were classified into three groups (typical AD (amnestic), atypical AD as posterior cortical atrophy (PCA) and logopenic progressive aphasia (LPA). Participants underwent baseline and 1-year follow-up structural MRI and flortaucipir tau-PET scans. Pittsburgh compound B (PiB) PET imaging was performed at baseline to determine amyloid-b (+) patients. Cognitively unimpaired amyloid-b (-) individuals acted as controls. Tau accumulation in frontal region with higher annual rates of accumulation was a specific biomarker for the two atypical AD variants. Involvement of temporal lobes differentiated PCA and LPA from cognitively unimpaired individuals. PCA participants differed from typical AD and LPA with higher rates of tau accumulation in the left lateral temporal and parietal regions and lower rates in the right occipital regions. LPA participants also differed from typical AD by higher annual rates of tau accumulation throughout the brain and in the right temporoparietal lobe. Atrophy in bilateral occipitotemporal regions differentiated PCA from healthy controls. For LPA, atrophy in left temporal and parietal regions were possible biomarkers. Sparing of hippocampus was noted for atypical AD, while involvement of medial temporal region was key regions for typical AD. In conclusion AD phenotype were characterised by different baseline and rates of change in tau pathology and grey matter loss, with some overlap particularly in the temporoparietal regions.
References:
Irene Sintini, Jonathan Graff-Radford, Matthew L. Senjem, Christopher G. Schwarz, Mary M. Machulda, Peter R. Martin, David T. Jones, Bradley F. Boeve, David S. Knopman, Kejal Kantarci, Ronald C. Petersen, Clifford R. Jack Jr, Val J. Lowe, Keith A. Josephs and Jennifer L. Whitwell. Longitudinal neuroimaging biomarkers differ across Alzheimer’s disease phenotypes. Brain. 2020; 2020:awaa155. doi: 10.1093/brain/awaa155. https://pubmed.ncbi.nlm.nih.gov/32572464/