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Anavex Life Sciences Highlights New Scientific Findings on Shared Biology Between Autism and Alzheimer’s Disease
Findings underpin the scientific rationale for Anavex’s targeted autophagy approach with orally administered blarcamesine Convergence of impaired autophagy
About this update from Anavex Life Sciences Corp.
[{"type":"text","content":"Findings underpin the scientific rationale for Anavex’s targeted autophagy approach with orally administered blarcamesine Convergence of impaired autophagy and synaptic dysfunction across neurodevelopmental and neurodegenerative conditions aligns with blarcamesine’s mechanism of action These findings support Anavex’s intent to advance blarcamesine into pivotal clinical studies to further evaluate its potential in addressing unexpectedly common CNS disease mechanisms NEW YORK, April 14, 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 new findings on the shared biology between autism spectrum disorder (ASD) and Alzheimer’s disease (AD), a core area of Anavex’ development plans with its autophagy enhancing orally administered blarcamesine. Key Highlights Multiple peer-reviewed publications point to biological link between autism spectrum disorder (ASD) and Alzheimer’s disease (AD), including shared disruptions in autophagy.Epidemiological data show that autistic adults may be diagnosed with Alzheimer’s and related dementias at rates up to 8 times higher than the general population, with onset occurring years or decades earlier than typical.Converging human genetic evidence links numerous high-confidence ASD risk genes — including TSC1/TSC2, PTEN, SHANK3, and FMRP — to impaired cellular autophagy, establishing autophagy dysfunction as a shared molecular substrate across genetically diverse forms of ASD.Synaptic dysfunction in ASD is now understood to arise, in substantial part, from a failure of autophagy-dependent synaptic pruning — causing an excess of poorly regulated synaptic connections and disrupted excitatory–inhibitory balance in neural circuits.The brain’s extracellular matrix (ECM) is pathologically altered in ASD and is bidirectionally coupled to autophagy.Restoration of autophagy impairment, now emerging as a central shared pathway in both ASD and AD, is precisely the biological system targeted by blarcamesine through its activation of SIGMAR1.Blarcamesine has demonstrated restorati...