Blarcamesine prevents cognitive decline in Alzheimer's disease model.

Anavex Life Sciences Corp. reported a peer-reviewed publication in Neuroscience Letters showing that pre-treatment with blarcamesine prevented Amyloid beta-induced memory impairment and brain oxidative injury, suggesting blarcamesine is an attractive candidate for Alzheimer's disease pharmacological prevention.

Anavex Life Sciences Corp. (Nasdaq: AVXL), a biopharmaceutical company specializing in neurodegenerative and neuropsychiatric disorders, has published a peer-reviewed study in Neuroscience Letters, titled "Prevention of memory impairment and hippocampal injury with blarcamesine in an Alzheimer's disease model" [1]. The study demonstrates that pre-treatment with blarcamesine, the company's lead drug candidate, entirely prevented amyloid beta-induced cognitive decline and brain oxidative injury in an animal model of Alzheimer's disease.

The study, conducted by Dr. Tangui Maurice of the University of Montpellier, France, and published in the journal Neuroscience Letters, shows that blarcamesine's ability to restore impaired autophagy through SIGMAR1 activation upstream of amyloid and tau pathologies at the molecular level is critical. This mechanism enhances autophagic flux and proteostasis capacity, potentially preventing the onset of Alzheimer's disease in healthy individuals [2].

In the study, mice pre-treated with blarcamesine showed significant protection against amyloid toxicity and oxidative stress, while placebo-controlled mice developed significant amyloid toxicity and memory deficits. This suggests that blarcamesine may be an attractive candidate for Alzheimer's disease pharmacological prevention.

Anavex's President and CEO, Christopher U Missling, PhD, commented on the findings, "These findings further support the potential beneficial effect of blarcamesine in Alzheimer's disease prevention. With once-daily oral blarcamesine administration and hence retaining autophagy strength through upstream SIGMAR1 activation, the downstream potentially pathological manifestations of Amyloid beta might be prevented."

The study highlights the potential of blarcamesine as a safe and effective pharmacologic agent for Alzheimer's disease prevention. The company's focus on SIGMAR1 activation and its potential to restore cellular homeostasis aligns with the growing understanding of the role of autophagy in neurodegenerative diseases.

References:
[1] Maurice, Tangui. “Prevention of memory impairment and hippocampal injury with blarcamesine in an Alzheimer's disease model.” Neuroscience letters, 138349. Aug. 2025. [https://pubmed.ncbi.nlm.nih.gov/40784611/](https://pubmed.ncbi.nlm.nih.gov/40784611/)
[2] Christ, M G et al. “Sigma-1 Receptor Activation Induces Autophagy and Increases Proteostasis Capacity In Vitro and In Vivo.” Cells vol. 8,3 211. 2 Mar. 2019. [https://www.mdpi.com/2073-4409/8/3/211](https://www.mdpi.com/2073-4409/8/3/211)