a(CHEBI:scopolamine)

Entity

Name

scopolamine

Namespace

chebi

Namespace Version

20180906

Namespace URL

https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/chebi-names.belns

This file encodes the article Activation of M1 and M4 muscarinic receptors as potential treatments for Alzheimer’s disease and schizophrenia by Choi et al, 2014

This document contains the curation of the review article Nicotinic receptors: allosteric transitions and therapeutic targets in the nervous system by Taly et al. 2009

Moreover, additional pre-clinical studies with TBPB demonstrated efficacy in reducing antipsychotic-like behaviors and in reversing scopolamine-impaired acquisition of contextual fear.59 Studies in cell lines also demonstrated that TBPB promoted a non-amyloidogenic pathway and decreased Abeta production, indicating that M1 modulation may have efficacy in the treatment of both symptomatic and pathologic features of AD PubMed:24511233

In brain slice electrophysiology studies, BQCA enhanced excitatory postsynaptic currents in medial prefrontal cortical neurons,69 an area critical for higher cognitive, learning, and memory functions.70 In pre-clinical animal studies, BQCA reversed scopolamine-impaired contextual fear conditioning and rescued medial prefrontal cortex-dependent discrimination reversal learning deficits in a transgenic mouse model of AD. PubMed:24511233

More recently, the M1-selective allosteric agonist VU0357017 was discovered, which displayed improved potency via binding to a novel allosteric site on the M1 mAChR. VU0357017 significantly blocked scopolamine-impaired contextual fear conditioning and enhanced spatial and contextual fear learning PubMed:24511233

As expected, AR-R17779 — a selective partial alpha7 nAChR agonist — improved scopolamine-elicited deficits in social recognition, and the 24-hour memory retention interval in unimpaired animals. Repeated doses of AR-R17779 enhanced long-term learning and attenuated working-memory deficits in rats. PubMed:19721446

Moreover, additional pre-clinical studies with TBPB demonstrated efficacy in reducing antipsychotic-like behaviors and in reversing scopolamine-impaired acquisition of contextual fear.59 Studies in cell lines also demonstrated that TBPB promoted a non-amyloidogenic pathway and decreased Abeta production, indicating that M1 modulation may have efficacy in the treatment of both symptomatic and pathologic features of AD PubMed:24511233