Clifford R. Jack

TL;DR: The goal was to develop cut points for amyloid positron emission tomography (PET), tau PET, flouro‐deoxyglucose (FDG) PET, and MRI cortical thickness.

TL;DR: Results support the radial unit hypothesis that different developmental mechanisms promote surface area expansion and increases in thickness and find evidence that brain structure is a key phenotype along the causal pathway that leads from genetic variation to differences in general cognitive function.

TL;DR: Differences in connectivity in Alzheimer’s disease can be explained by differences in dwell time in DMN sub-network configurations, rather than steady state connectivity magnitude, which may underlie the TF-fMRI findings that have been described in mild cognitive impairment and cognitively normal subjects who are at risk for Alzheimer's dementia.

TL;DR: Reduced AV-1451 binding in neuritic pathology compared to neurofibrillary tangles suggests that the maturity of tau pathology may affect AV- fourteen51 binding and suggests complexity in AV- 1451 binding.

TL;DR: An in-depth analysis of changes within subsystems within the default mode network are related to biomarker profiles across the Alzheimer’s disease spectrum and results support a cascading network failure model of Alzheimer's disease.