Anavex Therapies Reverse Cognitive Defects in Mice, Suggesting Their Use for Parkinson’s

Anavex Therapies Reverse Cognitive Defects in Mice, Suggesting Their Use for Parkinson’s

Anavex Life Sciences therapies reversed Alzheimer’s-related cognitive deficits in mice and improved processes connected with the disease, according to presentations at an international conference on Alzheimer’s and Parkinson’s.

The presentations at the 13th International Conference on Alzheimer’s & Parkinson’s Diseases dealt with the experimental treatments Anavex 2-73, Anavex 3-71, and Anavex 1-41.

Anavex 2-73, the company’s lead therapy, addresses the misfolded proteins involved in several neurodegenerative diseases. It works by targeting the sigma-1 and muscarinic protein receptors to return cells to a state of equilibrium.  Anavex Life Sciences recently completed a Phase 2a clinical trial of Anavex 2-73 for Alzheimer’s.

In pre-clinical trial studies, Anavex 2-73 showed promise in stopping and reversing Alzheimer’s progression. It also displayed anticonvulsant, anti-amnesic, neuroprotective and anti-depressant properties, suggesting it could be used to treat other diseases, such as epilepsy.

In 2015, the Michael J. Fox Foundation for Parkinson’s Research awarded Anavex Life Sciences a grant to study Anavex 2-73 in an animal model of Parkinson’s.

Another Anavex Life Sciences compound, Anavex 3-71, also targets the sigma-1 and M1 muscarinic receptors. It has shown promise in treating such Alzheimer’s hallmarks as cognitive deficits, accumulation of faulty beta-amyloid and tau proteins, nerve inflammation and defective mitochondrial activity.

Accumulation of the proteins are associated with Alzheimer’s. Mitochondria are cell components that convert food into energy. Their inability to produce enough energy in neurons is associated with neurodegenerative diseases.

Dr. Hélène Hall, a professor at McGill University, gave one of the presentations in Vienna. She said studies in mice with Alzheimer’s showed that Anavex 3-71 reduced inflammatory response in the brain and increased the formation of new contacts, or synapses, between brain neurons. A diminished number of those contacts is a hallmark of Alzheimer’s.

Hall’s study was titled “Targeting M1 Muscarinic And Sigma-1 Receptors In Alzheimer’s Disease: Reversal Of Pathological Hallmarks And Associated Cognitive Dysfunction In Mcgill-R-Thy1-APP Rats.”

Anavex 3-71 also decreased the accumulation of amyloid beta protein and reversed cognitive deficits in mice with Alzheimer’s. The reversal occurred despite the mice having an advanced stage of the disease.

Importantly, the results held after the body eliminated Anavex 3-71, a finding that appears to strengthen its therapeutic potential.

Nino Goguadze of the Université de Montpellier in France made another Anavex presentation. He said studies showed that, when amyloid beta was introduced in mice, Anavex 2-73, Anavex 3-71 and Anavex 1-41 protected mitochondrial activity.

His presentation was titled “The Dual Regulation Of Oxidative Stress By SIGMA1 Receptors In Physiological Or Pathological Conditions.”

“These new results provide converging evidence on mechanism of action as well as possible disease-modifying properties potentially by restoring homeostasis [a state of equilibrium] by means of the sigma-1 receptor agonists in our pipeline,” Christopher U. Missling, Anavex’s CEO, said in a news release. “This data also provides a foundation for our ongoing translational research efforts.”

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