Press release
Anavex Life Sciences Announces New Publication in Medical Journal: Blarcamesine Prevented Cognitive Impairment in Animal Model of Alzheimer’s Disease
Pre-Treatment with blarcamesine entirely prevented Abeta-induced cognitive decline Confirmed significant biomarker-response in hippocampus NEW YORK, Aug. 20,
About this update from Anavex Life Sciences Corp.
[{"type":"text","content":"Pre-Treatment with blarcamesine entirely prevented Abeta-induced cognitive decline Confirmed significant biomarker-response in hippocampus NEW YORK, Aug. 20, 2025 (GLOBE NEWSWIRE) -- Anavex Life Sciences Corp. (“Anavex” or the “Company”) (Nasdaq: AVXL), a clinical-stage biopharmaceutical company focused on developing innovative treatments for Alzheimer's disease, Parkinson's disease, schizophrenia, neurodevelopmental, neurodegenerative, and rare diseases, including Rett syndrome, and other central nervous system (CNS) disorders, today reported a peer-reviewed publication in the journal Neuroscience Letters, titled “Prevention of memory impairment and hippocampal injury with blarcamesine in an Alzheimer’s disease model.”1 This study shows that a pre-treatment with blarcamesine prevented Amyloid beta-induced memory impairment and brain oxidative injury suggesting that blarcamesine is an attractive candidate for Alzheimer's disease pharmacological prevention. “This preclinical study is exciting since it clearly demonstrates a preventative effect of blarcamesine in Alzheimer’s pathology and potentially might be able to prevent onset of Alzheimer's disease in healthy individuals,” said Tangui Maurice, PhD, Research Director at University of Montpellier, France and author of the publication. “These findings support the future direction of clinical trials with the objective of addressing blarcamesine’s potential as a safe and effective pharmacologic agent — applied as convenient once-daily oral pill — for the prevention of Alzheimer's disease.” While placebo-controlled mice developed significant amyloid toxicity in the brains after the toxic Aβ25-35 peptide injection, in animals pre-treated with blarcamesine, significant protection was observed with less vulnerability to Aβ25-35-induced oxidative stress and less vulnerability to develop learning and memory deficits. The mechanistic confirmation that blarcamesine particularly restores impaired autophagy through SIGMAR1 activation by acting upstream of amyloid and tau pathologies at the molecular level was previously established both in vitro and in vivo. Specifically, blarcamesine’s studies demonstrated effect of enhanced autophagic flux in human cells and in C. elegans as well as increased proteostasis capacity and ability to promote autophagosome biogenesis, autophagic cargo reception...