David G. Coughlin

TL;DR: Defining cell-specific stages of tau pathology helps to identify preclinical or early-stage cases for the better understanding of early pathogenic events, has implications for understanding the clinical subtype-specific dynamics of disease-propagation, and informs tau-neuroimaging on distribution patterns.

TL;DR: Using digital histology in a large autopsy cohort of Lewy body disorder patients with dementia to test the hypotheses that co‐occurring Alzheimer disease pathology impacts the anatomic distribution of α‐synuclein (SYN) pathology and that co-occurring neocortical tau pathology in LBDs associates with worse cognitive performance and occurs in a pattern differing from AD.

TL;DR: Higher antemortem CSF t-tau/Aβ1-42 and lower Aβ1/42 levels are predictive of increasing cerebral AD and SYN pathology, which may identify patients with LBD vulnerable to cortical SYn pathology who may benefit from both SYN and AD-targeted disease-modifying therapies.

TL;DR: The findings suggest that the astroglial “scar” in sclerotic MTLE has active, ongoing cellular changes, and targeting mTOR in MTLE may provide new pathways for the medical therapy of epilepsy.

TL;DR: It is proposed that Alzheimer's disease copathology is one of several likely pathological contributors to clinical heterogeneity of Lewy body disorders, and that such pathology can be assessed in vivo.