Mark P. Mattson

TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.

TL;DR: The recapitulation of salient features of AD in these mice clarifies the relationships between Abeta, synaptic dysfunction, and tangles and provides a valuable model for evaluating potential AD therapeutics as the impact on both lesions can be assessed.

TL;DR: Rapid progress towards understanding the cellular and molecular alterations that are responsible for the neuron's demise may soon help in developing effective preventative and therapeutic strategies in Alzheimer's disease.

TL;DR: The hypothesis that beta-amyloid can destabilize neuronal calcium regulation and render neurons more vulnerable to environmental stimuli that elevate intracellular calcium levels is tested.

TL;DR: Using electron microscopy and solid-state nuclear magnetic resonance measurements on fibrils formed by the 40-residue β-amyloid peptide of Alzheimer's disease (Aβ1–40), it is shown that different fibril morphologies have different underlying molecular structures, that the predominant structure can be controlled by subtle variations infibril growth conditions, and that both morphology and molecular structure are self-propagating when fibrs grow from preformed seeds.