Rik Vandenberghe

TL;DR: All patients carrying a loss-of-function mutation in ABCA7 exhibited a classical Alzheimer disease phenotype, though with a striking wide onset age range, suggesting the influence of unknown modifying factors.

TL;DR: WMH burden may impact on CC microstructure in late-onset depression suggesting vascular pathology has additional deleterious effects in these patients.

TL;DR: High educational attainment was associated with slower loss of grey matter over time in mutation carriers, demonstrating that even in presence of ongoing pathological processes, education may facilitate both brain reserve and brain maintenance in the presymptomatic phase of genetic FTD.

TL;DR: Evidence for presymptomatic impaired semantic knowledge in genetic FTD is provided and the different neuroanatomical associations of the mCCT score may represent distinct cognitive processes causing deficits in different groups: loss of core semantic knowledge associated with temporal lobe atrophy (particularly in the MAPT group), and impaired executive control of semantic information associated with frontal lobe atrocphy.

TL;DR: Results show that one aspect of Aβ pathology can be used to predict the other two, and correlates well with the development of dementia, advancing NFT and neuritic plaque pathology, andAmyloid PET-based estimates for staging of amyloid pathology indicate the progression status of ameloid pathology in general and, in doing so, also of AD pathology.