Anavex Life Sciences Corp. (NASDAQ: AVXL) announced that a University of California study published in Proceedings of the National Academy of Sciences, Nexus supports the hypothesis that autophagy impairment acts upstream of amyloid beta and tau pathology in Alzheimer's disease.

The study, titled "The microtubule nexus linking amyloid beta and tau: A simple and unifying theory for the underlying cause of Alzheimer's disease," proposes that amyloid beta disrupts tau's interaction with microtubules, leading to microtubule instability and abnormal tau phosphorylation. The authors conclude that autophagy failure associated with aging increases intracellular amyloid beta levels, contributing to the pathological cascade before extracellular plaques or neurofibrillary tangles form.

According to the research, autophagy normally clears proteins such as amyloid beta from cells, but this process slows with age, potentially allowing amyloid beta to accumulate and compete with tau for microtubule binding.

Anavex stated the findings align with its clinical data showing that blarcamesine, a SIGMAR1 activator, restores neural autophagy. "This new publication adds to the growing body of scientific data demonstrating that autophagy dysfunction is potentially an early and addressable factor contributing to the onset of Alzheimer's disease," said Christopher U. Missling, Anavex's president and chief executive officer.

The company's lead drug candidate blarcamesine has completed Phase 2a and Phase 2b/3 clinical trials for Alzheimer's disease, along with trials for Parkinson's disease dementia and Rett syndrome. The drug candidate targets SIGMAR1 and muscarinic receptors and is designed to restore cellular homeostasis.

Information in this article is based on a press release statement from Anavex Life Sciences Corp.