New publication on early- and late-onset AD atrophy patterns

New publication led by Anika Wuestefeld (accessible here) published in Alzheimer‘s Research & Therapy. It has been hypothesized that EOAD is medial temporal lobe (MTL) sparing. Yet, often EOAD is studied comprising various clinical phenotypes into one group. Given the importance of the MTL in memory, we tested if this assumption of lower MTL involvement in EOAD holds even for biomarker-defined amnestic EOAD.

First, to investigate the amygdala, we developed a new and reliable T1-weighted MRI segmentation protocol for the whole amygdala that has been incorporated into the existing ASHS atlas and which will be publicly available.

We compare the amnestic EOAD to controls and an amnestic late-onset AD group (aLOAD) for MTL subfield volume/thickness differences as well as pathologies such as tau, WMH, and a proxy of TDP-43 pathology. In line with our hypothesis, we see that MTL atrophy is present in amnestic EOAD and shows overall comparable levels to aLOAD. Additionally, also MTL tau-PET uptake and co-pathologies, such as a proxy for TDP-43, showed similar levels between aEOAD and aLOAD. In the paper are more additional analyses show (I) that aLOAD performs worse in verbal fluency and naming compared to aEOAD, (II) lower parietal thickness in aEOAD compared to aLOAD, (III) in exploratory analyses, differences to non-amnestic EOAD and LOAD groups.

We find that medial temporal lobe atrophy patterns in amnestic early-onset Alzheimer’s disease are similar to those of amnestic late-onset AD and show similar levels of co-pathologies. These results suggest that the driving mechanisms of the amnestic symptoms in both amnestic groups might be similar and resulting in similar atrophy patterns within the MTL.

Thanks to all participants of the BioFINDER study and all co-authors and collaborators for making this work possible.