Sally Hunter

TL;DR: A recently recognized brain disorder that mimics the clinical features of Alzheimer’s disease: Limbic-predominant Age-related TDP-43 Encephalopathy (LATE).

TL;DR: Multivariable analysis identified associations between dementia during life and entorhinal cortex neuritic plaques, hippocampal diffuse plaque, neocortical neurofibrillary tangles, white matter pallor, Lewy bodies, and hippocampal atrophy, which were consistent in those with clinical Alzheimer's disease.

TL;DR: It is clear that mild cognitive impairment is neuropathologically complex and cannot be understood within a single framework, and standardization of the definition of MCI and reporting of pathology would greatly assist in building an integrated picture of the clinical and neuropathological profile ofMCI.

TL;DR: The ACH, PSH and AMA in relation to levels of APP proteolytic fragments reported from AD-associated mutations in APP are reviewed and the confounding effects of sequence homology, complexity of competing cleavages and antibody cross reactivities all illustrate limitations in the understanding of the roles these fragments and the APP proteologic system as a whole in normal aging and disease play.

TL;DR: The senescence hypothesis of AD progression is presented, suggesting that factors associated with AD can be seen as partial stressors within the matrix of signalling pathways that underlie cell survival and function.