B. T. Hyman

TL;DR: These data support distinct processes in the initiation and progression of AD pathology within the temporal cortex: Deposition of Aβ reaches a “ceiling” early in the disease process, whereas NFT formation, synaptic loss, and gliosis continue throughout the course of the illness.

TL;DR: It is shown that the low density lipoprotein (LDL) receptor-related protein (LRP) is responsible for the endocytosis of secreted APP and this data link in a single metabolic pathway two molecules strongly implicated in the pathophysiology of AD.

TL;DR: The finding that manipulations of the carboxy-terminus of alpha-synuclein lead to inclusion formation may provide a model for studies of the pathogenic mechanisms ofalpha- synuclein aggregation in Lewy bodies, and be a tool for experimental manipulations to induce aggregate formation.

TL;DR: Analysis of a clinical series of patients with CAA-related hemorrhage confirmed an overrepresentation of APOE ϵ2 as well as an association between this allele and earlier age of first hemorrhage, suggesting that APOEϵ2 and ϵ4 might promote CAA’s hemorrhage through separate mechanisms.

TL;DR: Dramatic, focal neuronal toxicity associated primarily with thioflavin S-positive fibrillar Aβ deposits in both AD and PSAPP mice is found and suggests that Aβ develops neurotoxic properties in vivo when it adopts a fibrillsar β-pleated sheet conformation.