Anavex Life Sciences Corp (AVXL)

[polarbear77]

I concur. And great find Mycroft and Falconer.

The below was always one of my personal favorites:

https://www.anavex.com/newlypublished_data_alzheimer/

NEW YORK, NY – November 21, 2017 – New data published in the current issue of the peer-reviewed scientific journal Neurotoxicity Research[1] confirm that sigma-1 agonists, including multiple investigational compounds from Anavex Life Sciences Corp. (“Anavex” or the “Company”) (NASDAQ: AVXL), induce an anti-oxidant effect and protect mitochondrial function in pathological central nervous system conditions. In addition, another recent publication in the peer-reviewed scientific journal, Behavioural Brain Research[2], confirms that the absence of sigma-1 receptor function exacerbates amyloid toxicity and increases learning impairments in pharmacologic and genetic mouse models of Alzheimer’s disease.

Lead author of both publications, Tangui Maurice, PhD, Professor at INSERM Montpellier noted, “Both findings are consistent with the concept that sigma-1 receptor activity seems to be essential for cell survival under stress with the ability to counter the different manifestations of Alzheimer’s disease and other neurodegenerative pathologies.”

Mitochondrial dysfunction and oxidative damage are key factors involved in the pathology of many neurodegenerative diseases. Research shows that oxidative damage occurs in the brains of people with Alzheimer’s disease prior to the onset of significant plaque pathology [3].

The Neurotoxicity Research publication provides further insight on the mechanism of three Anavex sigma-1 receptor (S1R) agonists, ANAVEX®2-73, ANAVEX®1-41, and ANAVEX®3-71, which are all being studied in neurodegenerative diseases including Alzheimer’s disease (AD), Parkinson’s disease (PD) and multiple sclerosis (MS). Since S1R agonists are known to be potent neuroprotectants in preclinical models, they might play a critical role in providing neuroprotection for patients with AD and related disorders.

The second publication investigates how lack of S1R function effects learning behavior and biochemical markers in a pharmacologic and a genetic mouse model of AD. The transgenic mice, bred to express human amyloid precursor protein (APP) carrying the Swedish and Indiana mutations, APPSweInd (also known as the J20 line), were crossbred with S1R knockout (S1RKO) mice (APPSweInd/S1RKO). Compared to APPSweInd or S1RKO mice, APPSweInd/S1RKO exhibited an increased vulnerability to amyloid toxicity and more pronounced deficits in both short and long term memory. Furthermore, these deficits increased with age. Analyses of oxidative stress and Bax expression levels in the hippocampus of these animals also confirmed a higher level of toxicity in APPSweInd mouse brains when S1R expression had been deleted. These observations support the concept that S1R activity is a signal amplifier for endogenous neuroprotection systems.

“These results seem to further validate sigma-1 receptor agonism as a therapeutic target for the treatment of neurodegenerative diseases,“ stated Christopher U. Missling, PhD, President and Chief Executive Officer of Anavex. “We continue our research on sigma-1 receptor agonists in a variety of central nervous system disorders, with our lead candidate, ANAVEX®2-73, soon progressing to a late-stage clinical trial for Alzheimer’s disease after positive data in a Phase 2a study.”