Shirley ShiDu Yan

TL;DR: It is demonstrated that Aβ-binding alcohol dehydrogenase (ABAD) is a direct molecular link from Aβ to mitochondrial toxicity and the ABAD-Aβ interaction may be a therapeutic target in Alzheimer's disease.

TL;DR: These features of RAGE allow the receptor to propagate cellular dysfunction in a number of pathophysiologically relevant situations, most often dictated by the formation and persistence of ligands in the tissues.

TL;DR: Data are consistent with the hypothesis that AGE-RAGE interaction induces expression of VCAM-1 which can prime diabetic vasculature for enhanced interaction with circulating monocytes.

TL;DR: It is hypothesized that AGEs cause perturbation in a diverse group of diseases, such as diabetes, inflammation, neurodegeneration, and aging, and it is proposed that targeting this pathway may represent a logical step in the prevention/treatment of the sequelae of these disorders.

TL;DR: Differences in mitochondrial properties and function of synaptic vs. nonsynaptic mitochondrial populations in the transgenic mouse brain, which overexpresses the human mutant form of amyloid precursor protein and Aβ are identified to demonstrate the central importance of synaptic mitochondrial dysfunction relevant to the development of synaptic degeneration in AD.