Donald L. Price

TL;DR: The hypothesis that activation of N‐methyl‐D‐aspartic acid (NMDA) and non‐NMDA glutamate receptors (GluR) results in a spectrum of morphologically distinct phenotypes of neuronal death, with apoptosis and necrosis as its endpoints is tested and support the concept that degenerative phenotype of excitotoxically injured neurons are influenced by the degree of brain maturity and GluR subtype stimulation.

TL;DR: In this view, high, rather than limiting, levels of SOD1 may place motor neurons selectively at risk in FALS, and these findings offer further support for the view that the mutations confer a gain of adverse function.

TL;DR: A 650 kilobase yeast artificial chromosome that contains the entire, unrearranged 400 kb human APP gene into mouse embryonic stem (ES) cells by lipid–mediated transfection and this transgenic strategy may prove invaluable for the development of mouse models for AD and DS.

TL;DR: It is concluded, that APLP2 and APP can substitute for each other functionally functionally in vivo and are required for early postnatal development.

TL;DR: It is revealed that compromised accumulation of murine PS1 and PS2 derivatives resulting from overexpression of human PS1 occurs in a manner independent of endoproteolytic cleavage, consistent with a model in which the abundance of PS2 fragments is regulated coordinately by competition for limiting cellular factor(s).