NEW YORK, March 20, 2026 (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 announced that a new peer-reviewed study published by University of California in Proceedings of the National Academy of Sciences, Nexus1 (Shoff et al., 2026) supports the hypothesis that disruption of neuronal homeostasis—particularly autophagy impairment—acts upstream of amyloid beta (Aβ) and tau pathology in Alzheimer’s disease.
The publication, titled “The microtubule nexus linking amyloid beta and tau: A simple and unifying theory for the underlying cause of Alzheimer’s disease,” proposes a unified mechanistic framework in which Aβ competitively disrupts tau’s interaction with microtubules, leading to microtubule instability, abnormal tau phosphorylation, and subsequent aggregation.
The authors note that autophagy failure associated with aging increases intracellular Aβ levels, directly contributing to the pathological cascade. The publication concludes that pathology begins before extracellular plaques or neurofibrillary tangles are formed, positioning autophagy as a likely very early observable defect in Alzheimer’s disease.
The publication is also consistent with evidence that the brain’s recycling system slows with age. Autophagy normally clears proteins such as amyloid beta from cells. If that process slows in older adults, amyloid beta may accumulate and begin competing with tau for microtubule binding.
The authors further provide an explanation why amyloid plaques, or oligomers of Aβ, do not play a primary role, which allows for accommodation of the disconnect between the prevalence of plaques within the brain and cognitive status. Also, the role of apolipoprotein E (APOE) expression, being the largest genetic risk factor in sporadic Alzheimer’s disease could be explained. APOE is thought to influence Aβ trafficking, which could play an important role by increasing neuronal uptake of extracellular Aβ—thus defeating or competing with beneficial secretion.
These findings directly align with Anavex’s clinical and mechanistic data showing that blarcamesine, a selective SIGMAR1 activator, restores and enhances neural autophagy, addressing a central upstream defect in Alzheimer’s disease biology.2,3
“This new publication adds to the growing body of scientific data demonstrating that autophagy dysfunction is potentially and early and addressable factor contributing to the onset of Alzheimer’s disease. Their findings reinforce the mechanistic foundation of blarcamesine, which is designed to restore autophagy through activation of the SIGMAR1 pathway,” said Christopher U. Missling, PhD, President and Chief Executive Officer of Anavex. “We believe targeting this upstream defect might be essential for achieving consistent, disease-modifying clinical benefit.”
Anavex’s precision medicine approach recognizes that Alzheimer’s pathology is heterogeneous, but autophagy dysfunction represents a causative co-factor that precedes divergent downstream manifestations across patient subgroups.
The publication has been also discussed here.
This release discusses investigational uses of an agent in development and is not intended to convey conclusions about efficacy or safety. There is no guarantee that any investigational uses of such product will successfully complete clinical development or gain health authority approval.
About Anavex Life Sciences Corp.
Anavex Life Sciences Corp. (Nasdaq: AVXL) is a publicly traded biopharmaceutical company dedicated to the development of novel therapeutics for the treatment of neurodegenerative, neurodevelopmental, and neuropsychiatric disorders, including Alzheimer's disease, Parkinson's disease, schizophrenia, Rett syndrome, and other central nervous system (CNS) diseases, pain, and various types of cancer. Anavex's lead drug candidate, blarcamesine (ANAVEX®2-73), has successfully completed a Phase 2a and a Phase 2b/3 clinical trial for Alzheimer's disease, a Phase 2 proof-of-concept study in Parkinson's disease dementia, and both a Phase 2 and a Phase 3 study in adult patients and one Phase 2/3 study in pediatric patients with Rett syndrome. Blarcamesine is an orally available drug candidate designed to restore cellular homeostasis by targeting SIGMAR1 and muscarinic receptors. Preclinical studies demonstrated its potential to halt and/or reverse the course of Alzheimer's disease. Blarcamesine also exhibited anticonvulsant, anti-amnesic, neuroprotective, and anti-depressant properties in animal models, indicating its potential to treat additional CNS disorders, including epilepsy. The Michael J. Fox Foundation for Parkinson's Research previously awarded Anavex a research grant, which fully funded a preclinical study to develop blarcamesine for the treatment of Parkinson's disease. We believe that ANAVEX®3-71, which targets SIGMAR1 and M1 muscarinic receptors, is a promising clinical stage drug candidate demonstrating disease-modifying activity against the major hallmarks of Alzheimer's disease in transgenic (3xTg-AD) mice, including cognitive deficits, amyloid, and tau pathologies. In preclinical trials, ANAVEX®3-71 has shown beneficial effects on mitochondrial dysfunction and neuroinflammation. Further information is available at www.anavex.com. You can also connect with the Company on Twitter, Facebook, Instagram, and LinkedIn.
Forward-Looking Statements
Statements in this press release that are not strictly historical in nature are forward-looking statements. These statements are only predictions based on current information and expectations and involve a number of risks and uncertainties. Actual events or results may differ materially from those projected in any of such statements due to various factors, including the risks set forth in the Company’s most recent Annual Report on Form 10-K filed with the SEC. Readers are cautioned not to place undue reliance on these forward-looking statements, which speak only as of the date hereof. All forward-looking statements are qualified in their entirety by this cautionary statement and Anavex Life Sciences Corp. undertakes no obligation to revise or update this press release to reflect events or circumstances after the date hereof.
For Further Information:
Anavex Life Sciences Corp.
Research & Business Development
Toll-free: 1-844-689-3939
Email: info@anavex.com
Investors:
Andrew J. Barwicki
Investor Relations
Tel: 516-662-9461
Email: andrew@barwicki.com
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1 Shoff, AT et al. The microtubule nexus linking amyloid beta and tau: A simple and unifying theory for the underlying cause of Alzheimer's disease. PNAS Nexus, Volume 5, Issue 3, March 2026, pgag034.
2 Christ, MG, et al. Sigma-1 receptor activation induces autophagy and increases proteostasis capacity in vitro and in vivo. Cells. 2019;8(3):211.
3 Baeken, MW et al. Conserved LIR-specific interaction of Sigma-1 receptor and GABARAP. iScience vol. 28,9 113287. 5 Aug. 2025.
