Leland Stanford Junior University

Ronald J Weigel

William C Mobley

Har Hiu Dawn Lam

Chengbiao Wu

Neurological dysfunction is prevented or treated by the administration of ligands that activate the GPR30 receptor. Ligands include estrogens and structurally related molecules. Preferably the GPR30 ligand is an orally available drug that can cross into the brain from blood. Screening methods are provided for ligands that do not activate other estrogen receptors, and therefore do not have the classical estrogenic effects attributable to these receptors.

Use of GPR30 receptor ligands to mediate neurotrophic action

Neurological dysfunction is prevented or treated by the administration of ligands that activate the GPR30 receptor. Ligands include, but are not limited to, estrogens and structurally related molecules. In a preferred embodiment, the GPR30 ligand is an orally available drug that can cross into the brain from blood. Of particular interest are ligands that do not activate other estrogen receptors, and therefore do not have the classical estrogenic effects attributable to these receptors.

Method of screening for neuroprotective agents

ERF-1 is shown to be a transcriptional regulator of the expression of the estrogen receptor, where elevated ERF-1 is related to elevated expression of the estrogen receptor. By monitoring the level of ERF-1, one can relate phenotypic characteristics of carcinomas expressing ERF-1 as prognostic of the response of the tumor to various therapies. In addition, ERF-1 may be used for screening therapeutic drugs which may act as antagonists to initiation of estrogen receptor transcription.

Growing community of inventors

Woodside, CA, United States of America

Ronald J Weigel