Murali Gopalakrishnan

TL;DR: This review aims to provide an understanding of K(+) channel function at the molecular level in the context of disease processes and discuss the progress, hurdles, challenges, and opportunities in the exploitation of K(* channels as therapeutic targets by pharmacological and emerging genetic approaches.

TL;DR: Two distinct α7 PAM profiles are revealed, which could offer unique opportunities for modulating α7 nAChRs in vivo and in the development of novel therapeutics for central nervous system indications.

TL;DR: Data support the notion that α7 nAChR allosteric modulation may constitute a novel pharmacological principle for the treatment of cognitive dysfunction.

TL;DR: The recent discovery of chemically heterogeneous group of molecules capable of differentially modifying nAChR properties without interacting at the ligand binding site illustrates the adequacy of the allosteric model to predict functional consequences.

TL;DR: It is demonstrated that α7 nAChR agonism can lead to broad-spectrum efficacy in animal models at doses that enhance ERK1/2 and CREB phosphorylation/activation and may represent a mechanism that offers potential to improve cognitive deficits associated with neurodegenerative and psychiatric diseases, such as Alzheimer's disease and schizophrenia.