{"id":951094,"date":"2026-04-14T07:33:49","date_gmt":"2026-04-14T11:33:49","guid":{"rendered":"https:\/\/www.marketnewsdesk.com\/index.php\/anavex-life-sciences-highlights-new-scientific-findings-on-shared-biology-between-autism-and-alzheimers-disease\/"},"modified":"2026-04-14T07:33:49","modified_gmt":"2026-04-14T11:33:49","slug":"anavex-life-sciences-highlights-new-scientific-findings-on-shared-biology-between-autism-and-alzheimers-disease","status":"publish","type":"post","link":"https:\/\/www.marketnewsdesk.com\/index.php\/anavex-life-sciences-highlights-new-scientific-findings-on-shared-biology-between-autism-and-alzheimers-disease\/","title":{"rendered":"Anavex Life Sciences Highlights New Scientific Findings on Shared Biology Between Autism and Alzheimer\u2019s Disease"},"content":{"rendered":"<div class=\"mw_release\">\n<p align=\"center\">\n        <em>Findings underpin the scientific rationale for Anavex\u2019s targeted autophagy approach with orally administered blarcamesine<\/em>\n      <\/p>\n<p align=\"center\">\n        <em>Convergence of impaired autophagy and synaptic dysfunction across neurodevelopmental and neurodegenerative conditions aligns with blarcamesine\u2019s mechanism of action<\/em>\n      <\/p>\n<p align=\"center\">\n        <em>These findings support Anavex\u2019s intent to advance blarcamesine into pivotal clinical studies to further evaluate its potential in addressing unexpectedly common CNS disease mechanisms<\/em>\n      <\/p>\n<p align=\"justify\">NEW YORK, April  14, 2026  (GLOBE NEWSWIRE) &#8212; Anavex Life Sciences Corp. (\u201cAnavex\u201d or the \u201cCompany\u201d) (Nasdaq: AVXL), a clinical-stage biopharmaceutical company focused on developing innovative treatments for Alzheimer\u2019s disease, Parkinson\u2019s 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\u2019s disease (AD), a core area of Anavex\u2019 development plans with its autophagy enhancing orally administered blarcamesine.<\/p>\n<p align=\"justify\">\n        <strong><br \/>\n          <em>Key Highlights<\/em><br \/>\n        <\/strong>\n      <\/p>\n<ul type=\"disc\">\n<li style=\"margin-bottom:5pt;text-align:justify\">Multiple peer-reviewed publications point to biological link between autism spectrum disorder (ASD) and Alzheimer\u2019s disease (AD), including shared disruptions in autophagy.<\/li>\n<li style=\"margin-bottom:5pt;text-align:justify\">Epidemiological data show that autistic adults may be diagnosed with Alzheimer\u2019s and related dementias at rates up to 8 times higher than the general population, with onset occurring years or decades earlier than typical.<\/li>\n<li style=\"margin-bottom:5pt;text-align:justify\">Converging human genetic evidence links numerous high-confidence ASD risk genes \u2014 including TSC1\/TSC2, PTEN, SHANK3, and FMRP \u2014 to impaired cellular autophagy, establishing autophagy dysfunction as a shared molecular substrate across genetically diverse forms of ASD.<\/li>\n<li style=\"margin-bottom:5pt;text-align:justify\">Synaptic dysfunction in ASD is now understood to arise, in substantial part, from a failure of autophagy-dependent synaptic pruning \u2014 causing an excess of poorly regulated synaptic connections and disrupted excitatory\u2013inhibitory balance in neural circuits.<\/li>\n<li style=\"margin-bottom:5pt;text-align:justify\">The brain\u2019s extracellular matrix (ECM) is pathologically altered in ASD and is bidirectionally coupled to autophagy.<\/li>\n<li style=\"margin-bottom:5pt;text-align:justify\">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.<\/li>\n<li style=\"margin-bottom:5pt;text-align:justify\">Blarcamesine has demonstrated restoration of autophagy through SIGMAR1 activation in preclinical models and has shown clinical effects in Phase IIb\/III trials in early Alzheimer\u2019s disease, Phase II\/III in Rett syndrome (a neurodevelopmental disorder caused by MECP2 mutation), and Phase II in Parkinson\u2019s disease dementia.<\/li>\n<li style=\"margin-bottom:5pt;text-align:justify\">Collectively, these data provide a scientific basis for advancing blarcamesine into pivotal clinical studies, subject to further evaluation and regulatory considerations.\n<\/li>\n<\/ul>\n<p align=\"justify\">\n        <strong><br \/>\n          <em>Reframing Brain Disorders: Converging Pathways in Neurodevelopment and Neurodegeneration<\/em><br \/>\n        <\/strong>\n      <\/p>\n<p align=\"justify\">For decades, autism and Alzheimer\u2019s disease were treated as conditions on opposite ends of the lifespan \u2014 one affecting brain development in early childhood, the other driving decline in old age. New research is adding a critical new twist. A landmark April 2025 study published in JAMA analyzed Medicare and Medicaid records covering more than 114,000 autistic adults and found that dementia prevalence among this population was dramatically elevated compared to the general population.\u00b9 A separate recent 2026 paper in Frontiers in Neuroscience identified convergent disruptions in two critical systems shared by both conditions: The autophagy network and the synaptic regulation machinery.\u00b2<\/p>\n<p align=\"justify\">Autophagy is the cell\u2019s natural process for clearing misfolded proteins, damaged organelles, lipids, and other cellular waste. In autism, excess synaptic connections form which are not properly pruned during development. In Alzheimer\u2019s disease, impaired autophagy, worsened by ApoE4 lipoproteins, allows toxic protein aggregates \u2014 including amyloid-beta and fibrillary tau \u2014 to accumulate unchecked. Both conditions, in essence, share a common driver of disease pathogenesis: A failure of the brain\u2019s housekeeping system.<\/p>\n<p align=\"justify\">\n        <strong><br \/>\n          <em>Synaptic Dysfunction in ASD: When the Brain\u2019s Pruning Mechanism Fails<\/em><br \/>\n        <\/strong>\n      <\/p>\n<p align=\"justify\">The human brain is sculpted by a process of exuberant synapse formation followed by selective elimination \u2014 synaptic pruning \u2014 that removes excess connections and renders neural circuits fully functional. Autophagy is a core cellular mechanism enabling this pruning. A landmark Neuron study\u00b3 found excess dendritic spines in postmortem ASD cortical tissue compared to controls \u2014 direct evidence of failed pruning correlating with impaired autophagy. Blocking neural autophagy genetically reproduced core ASD features: Excess synapse density, impaired social behavior, and repetitive behaviors; restoring autophagy normalized both synaptic architecture and behavior. Microglia, the brain\u2019s resident immune cells, depend equally on autophagy for synapse elimination.\u2074 The downstream consequence of both failures is a disruption of excitatory\u2013inhibitory balance \u2014 a core pathobiological signature of ASD.\u2075<sup>,<\/sup>\u2076<\/p>\n<p align=\"justify\">\n        <strong><br \/>\n          <em>The Genetic Architecture of ASD Converges on Autophagy<\/em><br \/>\n        <\/strong>\n      <\/p>\n<p align=\"justify\">ASD is genetically heterogeneous, yet genome analyses repeatedly converge on a common theme: Mutations and copy-number variants in genes whose protein products regulate autophagy. Among the most studied are mutations in TSC1\/TSC2 and PTEN genes, whose loss of function suppresses autophagy and is associated with high rates of ASD alongside epilepsy and intellectual disability.\u2077\u00a0Fragile-X syndrome \u2014 the most common inherited cause of intellectual disability and autism \u2014 likewise involves reduced autophagic flux in hippocampal neurons, with activation of autophagy rescuing aberrant spine morphology, synaptic plasticity, and cognition in preclinical models.\u2075 SHANK3 mutations further alter autophagy-dependent protein homeostasis at the synapse.\u2078\u00a0Whole-exome sequencing has additionally identified copy-number variants in core autophagy genes in sporadic ASD cases.\u2079 This genetic convergence is not coincidental; it is pathobiologically instructive.<\/p>\n<p align=\"justify\">\n        <strong><br \/>\n          <em>The Brain\u2019s Extracellular Matrix and Autophagy: A Bidirectional Relationship<\/em><br \/>\n        <\/strong>\n      <\/p>\n<p align=\"justify\">A third dimension of ASD biology is receiving growing attention: The extracellular matrix (ECM) \u2014 the structural scaffold of proteins and proteoglycans surrounding all brain cells. Its most specialized form, the perineuronal net (PNN), enwraps key inhibitory interneurons and governs critical-period synaptic plasticity and circuit stability.\u00b9\u2070 PNN architecture is consistently altered in genetic ASD mouse models and in postmortem human ASD brain tissue.\u00b9\u00b9<sup>,<\/sup>\u00b9\u00b2 The ECM and autophagy are bidirectionally coupled: The ECM modulates intracellular autophagic activity, while autophagic flux is required for normal ECM remodeling and synaptic structural integrity.\u00b9\u00b3<sup>,<\/sup>\u00b9\u2074<sup>,<\/sup>\u00b9\u2075\u00a0PNN disruption has also been identified as relevant for Alzheimer\u2019s disease,\u00b9\u2076 reinforcing that the brain\u2019s ECM is not a passive structural scaffold but an active participant in the same homeostatic networks that autophagy governs \u2014 and that blarcamesine targets through SIGMAR1 activation.<\/p>\n<p align=\"justify\">\n        <strong><br \/>\n          <em>Why This Matters for Anavex and Blarcamesine<\/em><br \/>\n        <\/strong>\n      <\/p>\n<p align=\"justify\">Blarcamesine is an investigational oral therapy that activates SIGMAR1, a key intracellular chaperone protein that sits at a critical junction of cellular homeostasis. Peer-reviewed research has established that SIGMAR1 activation by blarcamesine restores impaired autophagy by stimulating ULK1 phosphorylation \u2014 a central signaling node that initiates the formation of autophagosomes, the cellular organelles responsible for engulfing and recycling damaged proteins and organelles.<\/p>\n<p align=\"justify\">This mechanism was first demonstrated at the molecular level in a 2019 publication in Cells, which showed that blarcamesine enhances autophagic flux in human cells and increases proteostasis capacity in the roundworm <em>C. elegans<\/em>, ultimately rescuing the organism from paralysis caused by protein aggregation.\u00b9\u2077 A 2025 iScience publication further elucidated the molecular protein binding mechanism of blarcamesine to SIGMAR1 and GABARAP, a core autophagy protein.\u00b9\u2078<\/p>\n<p align=\"justify\">The emerging picture of ASD \u2014 as a condition with co-contribution of autophagy failure, synaptic pruning deficits, convergent genetic disruption of protein homeostasis pathways, and ECM dysregulation \u2014 maps directly onto the disease biology that blarcamesine is designed to address. The therapeutic rationale is not inferential; it is mechanistically grounded in the same autophagic machinery that blarcamesine has been shown to restore across multiple model systems and in human clinical trials.<\/p>\n<p align=\"justify\">\n        <strong><br \/>\n          <em>Clinical Evidence Across the Lifespan<\/em><br \/>\n        <\/strong>\n      <\/p>\n<p align=\"justify\">Anavex\u2019s clinical development program spans both neurodegenerative and neurodevelopmental conditions, reflecting precisely the kind of cross-lifespan therapeutic strategy that the emerging autism\u2013Alzheimer\u2019s research now suggests is needed:<\/p>\n<p align=\"justify\">\n        <strong>Alzheimer\u2019s Disease: <\/strong>In the Phase IIb\/III ANAVEX<sup>\u00ae<\/sup>2-73-AD-004 trial, once-daily oral blarcamesine significantly slowed cognitive and functional decline in patients with early Alzheimer\u2019s disease over 48 weeks, supported by biomarker evidence including improved plasma A\u03b242\/40 ratio and significant reduction in brain atrophy in key brain areas. A precision medicine approach demonstrated that patients carrying wild-type SIGMAR1 (the ABCLEAR1 population, representing approximately 70% of the global population) showed enhanced clinical responses. This approach was further amplified in the ABCLEAR3 population, including the brain\u2019s extracellular matrix (ECM) wild-type protein COL24A1.<\/p>\n<p align=\"justify\">\n        <strong>Rett Syndrome: <\/strong>The AVATAR trial demonstrated clinical effects in adult patients with Rett syndrome, a severe neurodevelopmental disorder caused by mutations in the MECP2 gene \u2014 one of the genes now identified as key for brain development. Treatment was associated with changes in disease-relevant biomarkers, including a significant increase in GABA levels. Open-label extension data indicated disease-modifying effects. A Phase II\/III pediatric trial (EXCELLENCE) has also been completed.<\/p>\n<p align=\"justify\">\n        <strong>Parkinson\u2019s Disease Dementia: <\/strong>Blarcamesine has shown proof-of-concept efficacy in a Phase II study in Parkinson\u2019s disease dementia, a condition also linked to impaired autophagy and protein aggregation (alpha-synuclein). Advanced clinical development in Parkinson\u2019s disease is ongoing.<\/p>\n<p align=\"justify\">\u201cThe growing recognition that neurodevelopmental and neurodegenerative conditions share fundamental disease biology \u2014 particularly around autophagy \u2014 validates the foundational science behind Anavex\u2019s platform,\u201d said Wolfgang Liedtke, MD, PhD, Senior Vice President and Global Head of Neurology at Anavex. \u201cWe are looking forward to proceeding with pivotal clinical trials on the principle that restoring cellular homeostasis through SIGMAR1 activation may address disease biology across the CNS, from childhood through old age.\u201d<\/p>\n<p align=\"justify\">\u201cAs independent researchers from institutions including Mount Sinai, Boston University, Drexel University, and the Karolinska Institute continue to map the molecular connections between autism and Alzheimer\u2019s, the therapeutic rationale for a precision medicine approach targeting autophagy with blarcamesine has never been more encouraging,\u201d said Christopher U. Missling, PhD, President and Chief Executive Officer of Anavex. \u201cAnavex\u2019s unique precision medicine approach recognizes autophagy dysfunction as a common upstream contributor preceding diverse downstream pathologies across the age spectrum.\u201d<\/p>\n<p align=\"justify\">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.<\/p>\n<p>\n        <strong>About Anavex Life Sciences Corp.<\/strong>\n      <\/p>\n<p align=\"justify\">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&#8217;s disease, Parkinson&#8217;s disease, schizophrenia, Rett syndrome, and other central nervous system (CNS) diseases, pain, and various types of cancer. Anavex&#8217;s lead drug candidate, blarcamesine (<em>ANAVEX<sup>\u00ae<\/sup>2-73<\/em>), has successfully completed a Phase 2a and a Phase 2b\/3 clinical trial for Alzheimer&#8217;s disease, a Phase 2 proof-of-concept study in Parkinson&#8217;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&#8217;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&#8217;s Research previously awarded Anavex a research grant, which fully funded a preclinical study to develop blarcamesine for the treatment of Parkinson&#8217;s disease. We believe that ANAVEX<sup>\u00ae<\/sup>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&#8217;s disease in transgenic (3xTg-AD) mice, including cognitive deficits, amyloid, and tau pathologies. In preclinical trials, ANAVEX<sup>\u00ae<\/sup>3-71 has shown beneficial effects on mitochondrial dysfunction and neuroinflammation. Further information is available at <a href=\"https:\/\/www.globenewswire.com\/Tracker?data=h5ihOJEU3exBwJCB9erw533-sampY4LGvI0B2aXmeMdXbKyObM3OnOB6nsje27UF6zKOvH474i1GYrNgIC7wgA==\" rel=\"nofollow\" target=\"_blank\">www.anavex.com<\/a>. You can also connect with the Company on <a href=\"https:\/\/www.globenewswire.com\/Tracker?data=Wqdg6p1SdNLbFX6WL9qpL6NF0a0hfg9gAbCiH6ZbDQmTqJC2l6avQ6KbWkxz6pcxSS5K0zwpz6PTes0CjWjmPir7xMez_WljAOMjfKaiV-w=\" rel=\"nofollow\" target=\"_blank\">Twitter,<\/a><a href=\"https:\/\/www.globenewswire.com\/Tracker?data=8pjZU6JygxoejnY2ZUIh3hEV7LFInh7bE1eLrd70iOLmVibQeXNHaIRU3afBJR4XoQoaqPzkwNinutSH1-JSPZAjZbsGOyXbR7wDfb-i51HtbG3Nc1np5XD6h-eSaQvpndqyAOArwl5KsIp-bZ4lGA==\" rel=\"nofollow\" target=\"_blank\">Facebook<\/a>, <a href=\"https:\/\/www.globenewswire.com\/Tracker?data=Db3_dM_Z3LwQ2KeVx5uooJ6KdBM9zp1WvAEpjmokKmx1LiR-MvQuYpbPdAJHr61F8W_MYnnAVSSBu_VdgcY5OsoEDQdJMjNUlR-Hcis3sOY=\" rel=\"nofollow\" target=\"_blank\">Instagram<\/a>, and <a href=\"https:\/\/www.globenewswire.com\/Tracker?data=prFh6-M4WJQoTuznz5nyfbotKF-9qwDSiW92tgFq5W2OFMcRrcq9-jYElQSXtV8QBMK6xR4xDwCZYCFGeE_remUWz21wRjzY7BOtd9QJYkMTsmHkUPQdCqiooqDiMucj\" rel=\"nofollow\" target=\"_blank\">LinkedIn<\/a>.<\/p>\n<p>\n        <strong>Forward-Looking Statements<\/strong>\n      <\/p>\n<p align=\"justify\">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\u2019s 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.<\/p>\n<p align=\"justify\">\n        <strong>For Further Information:<\/strong><br \/>\n        <br \/>Anavex Life Sciences Corp.<br \/>Research &amp; Business Development<br \/>Toll-free: 1-844-689-3939<br \/>Email: <a href=\"https:\/\/www.globenewswire.com\/Tracker?data=cHcZdSK-GLhpxJqzc7b0pja1-XGdmokoTY_yrIDitNbP0U0_oW6A-J5WazBAWVF3djKnVoi053CxPqTFz-D9EbguPM2-EyljToUhR-sY1rQ=\" rel=\"nofollow\" target=\"_blank\">info@anavex.com<\/a><\/p>\n<p align=\"justify\">\n        <strong>Investors:<\/strong><br \/>\n        <br \/>Andrew J. Barwicki<br \/>Investor Relations<br \/>Tel: 516-662-9461<br \/>Email: <a href=\"https:\/\/www.globenewswire.com\/Tracker?data=f_KoM8yfBmPiM1ohoBAEDcqLRKxAhTMPWNSy2v4mHWLbQld8SBR8ajQ54eAyikqKL7EqhYE73d0ZeYd39xKuJ8fl1lZb48nAGBlsyV0Uvrc=\" rel=\"nofollow\" target=\"_blank\">andrew@barwicki.com<\/a><\/p>\n<p>\n        <strong>References<\/strong>\n      <\/p>\n<ol>\n<li>Vivanti G et al. \u201cPrevalence of Dementia Among US Adults With Autism Spectrum Disorder.\u201d JAMA Network Open. 2025;8(1):e2453691.<\/li>\n<li>Phillips WT et al. \u201cPathophysiologic similarities between autism spectrum disorder and Alzheimer\u2019s disease: therapeutic possibilities.\u201d Frontiers in Neuroscience. 2026;19:1737007.<\/li>\n<li>Tang G et al. \u201cLoss of mTOR-dependent macroautophagy causes autistic-like synaptic pruning deficits.\u201d Neuron. 2014;83(5):1131\u20131143.<\/li>\n<li>Kim HJ et al. \u201cDeficient autophagy in microglia impairs synaptic pruning and causes social behavioral defects.\u201d Molecular Psychiatry. 2017;22(11):1576\u20131584.<\/li>\n<li>Yan J et al. \u201cActivation of autophagy rescues synaptic and cognitive deficits in fragile X mice.\u201d PNAS. 2018;115(41):E9707\u2013E9716.<\/li>\n<li>Hui KK et al. \u201cGABARAPs dysfunction by autophagy deficiency in adolescent brain impairs GABA\u2081 receptor trafficking and social behavior.\u201d Sci Adv. 2019;5(4):eaau8237.<\/li>\n<li>Kwon CH et al. \u201cPten regulates neuronal arborization and social interaction in mice.\u201d Neuron. 2006;50(3):377\u2013388.<\/li>\n<li>Bourgeron T. \u201cA synaptic trek to autism.\u201d Curr Opin Neurobiol. 2009;19(2):231\u2013234.<\/li>\n<li>Dere E et al. \u201cHeterozygous ambra1 deficiency in mice: a genetic trait with autism-like behavior restricted to the female gender.\u201d Front Behav Neurosci. 2014;8:181.<\/li>\n<li>Fawcett JW et al. \u201cThe roles of perineuronal nets and the perinodal extracellular matrix in neuronal function.\u201d Nat Rev Neurosci. 2019;20(8):451\u2013465.<\/li>\n<li>Burket JA et al. \u201cRegion-Specific Alterations of Perineuronal Net Expression in Postmortem Autism Brain Tissue.\u201d Front Psychiatry. 2022;13:872615.<\/li>\n<li>Adeyelu TT et al. \u201cBehavioral regulation by perineuronal nets in the prefrontal cortex of the CNTNAP2 mouse model of autism spectrum disorder.\u201d Front Behav Neurosci. 2023;17:1114789.<\/li>\n<li>Fung C et al. \u201cInduction of Autophagy during Extracellular Matrix Detachment Promotes Cell Survival.\u201d Mol Biol Cell. 2008;19(3):797\u2013806.<\/li>\n<li>Bhatt DL et al. \u201cCooperation of cell adhesion and autophagy in the brain: Functional roles in development and neurodegenerative disease.\u201d Autophagy Reports. 2021;1(1):192\u2013222.<\/li>\n<li>Iozzo RV et al. \u201cInstructive Roles of Extracellular Matrix on Autophagy.\u201d Mol Cell Biol. 2014;34(22):4001\u20134012.<\/li>\n<li>Vries LE et al. \u201cResilience to Alzheimer\u2019s disease associates with alterations in perineuronal nets.\u201d Alzheimer\u2019s &amp; Dementia. 2025.<\/li>\n<li>Christ MG et al. \u201cSigma-1 receptor activation induces autophagy and increases proteostasis capacity in vitro and in vivo.\u201d Cells. 2019;8(3):211.<\/li>\n<li>Baeken MW et al. \u201cConserved LIR-specific interaction of Sigma-1 receptor and GABARAP.\u201d iScience. 2025;28(9):113287.<\/li>\n<\/ol>\n<p>      <img decoding=\"async\" alt=\"\" class=\"__GNW8366DE3E__IMG\" src=\"https:\/\/www.globenewswire.com\/newsroom\/ti?nf=OTY4OTAwMCM3NTMzMzc5IzIwMTk1Mzk=\" \/><br \/>\n      <br \/>\n      <img decoding=\"async\" alt=\"\" src=\"https:\/\/ml.globenewswire.com\/media\/YWQwOTQ0NDQtZDE0Yi00YzU5LWEwNzktYjk4ZDE2YTY2MWI0LTEwMzExNzYtMjAyNi0wNC0xNC1lbg==\/tiny\/Anavex-Life-Sciences-Corp-.png\" \/>\n    <\/div>\n<div class=\"mw_contactinfo\"><\/div>\n","protected":false},"excerpt":{"rendered":"<p>Findings underpin the scientific rationale for Anavex\u2019s targeted autophagy approach with orally administered blarcamesine Convergence of impaired autophagy and synaptic dysfunction across neurodevelopmental and neurodegenerative conditions aligns with blarcamesine\u2019s mechanism of action These findings support Anavex\u2019s 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) &#8212; Anavex Life Sciences Corp. (\u201cAnavex\u201d or the \u201cCompany\u201d) (Nasdaq: AVXL), a clinical-stage biopharmaceutical company focused on developing innovative treatments for Alzheimer\u2019s disease, Parkinson\u2019s 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\u2019s disease &hellip; <\/p>\n<p class=\"link-more\"><a href=\"https:\/\/www.marketnewsdesk.com\/index.php\/anavex-life-sciences-highlights-new-scientific-findings-on-shared-biology-between-autism-and-alzheimers-disease\/\" class=\"more-link\">Continue reading<span class=\"screen-reader-text\"> &#8220;Anavex Life Sciences Highlights New Scientific Findings on Shared Biology Between Autism and Alzheimer\u2019s Disease&#8221;<\/span><\/a><\/p>\n","protected":false},"author":2,"featured_media":0,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[],"tags":[],"class_list":["post-951094","post","type-post","status-publish","format-standard","hentry"],"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v27.4 - https:\/\/yoast.com\/product\/yoast-seo-wordpress\/ -->\n<title>Anavex Life Sciences Highlights New Scientific Findings on Shared Biology Between Autism and Alzheimer\u2019s Disease - Market Newsdesk<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/www.marketnewsdesk.com\/index.php\/anavex-life-sciences-highlights-new-scientific-findings-on-shared-biology-between-autism-and-alzheimers-disease\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Anavex Life Sciences Highlights New Scientific Findings on Shared Biology Between Autism and Alzheimer\u2019s Disease - Market Newsdesk\" \/>\n<meta property=\"og:description\" content=\"Findings underpin the scientific rationale for Anavex\u2019s targeted autophagy approach with orally administered blarcamesine Convergence of impaired autophagy and synaptic dysfunction across neurodevelopmental and neurodegenerative conditions aligns with blarcamesine\u2019s mechanism of action These findings support Anavex\u2019s 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) &#8212; Anavex Life Sciences Corp. (\u201cAnavex\u201d or the \u201cCompany\u201d) (Nasdaq: AVXL), a clinical-stage biopharmaceutical company focused on developing innovative treatments for Alzheimer\u2019s disease, Parkinson\u2019s 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\u2019s disease &hellip; Continue reading &quot;Anavex Life Sciences Highlights New Scientific Findings on Shared Biology Between Autism and Alzheimer\u2019s Disease&quot;\" \/>\n<meta property=\"og:url\" content=\"https:\/\/www.marketnewsdesk.com\/index.php\/anavex-life-sciences-highlights-new-scientific-findings-on-shared-biology-between-autism-and-alzheimers-disease\/\" \/>\n<meta property=\"og:site_name\" content=\"Market Newsdesk\" \/>\n<meta property=\"article:published_time\" content=\"2026-04-14T11:33:49+00:00\" \/>\n<meta property=\"og:image\" content=\"https:\/\/www.globenewswire.com\/newsroom\/ti?nf=OTY4OTAwMCM3NTMzMzc5IzIwMTk1Mzk=\" \/>\n<meta name=\"author\" content=\"Newsdesk\" \/>\n<meta name=\"twitter:card\" content=\"summary_large_image\" \/>\n<meta name=\"twitter:label1\" content=\"Written by\" \/>\n\t<meta name=\"twitter:data1\" content=\"Newsdesk\" \/>\n\t<meta name=\"twitter:label2\" content=\"Est. reading time\" \/>\n\t<meta name=\"twitter:data2\" content=\"12 minutes\" \/>\n<script type=\"application\/ld+json\" class=\"yoast-schema-graph\">{\"@context\":\"https:\\\/\\\/schema.org\",\"@graph\":[{\"@type\":\"Article\",\"@id\":\"https:\\\/\\\/www.marketnewsdesk.com\\\/index.php\\\/anavex-life-sciences-highlights-new-scientific-findings-on-shared-biology-between-autism-and-alzheimers-disease\\\/#article\",\"isPartOf\":{\"@id\":\"https:\\\/\\\/www.marketnewsdesk.com\\\/index.php\\\/anavex-life-sciences-highlights-new-scientific-findings-on-shared-biology-between-autism-and-alzheimers-disease\\\/\"},\"author\":{\"name\":\"Newsdesk\",\"@id\":\"https:\\\/\\\/www.marketnewsdesk.com\\\/#\\\/schema\\\/person\\\/482f27a394d4fda80ecb5499e519d979\"},\"headline\":\"Anavex Life Sciences Highlights New Scientific Findings on Shared Biology Between Autism and Alzheimer\u2019s Disease\",\"datePublished\":\"2026-04-14T11:33:49+00:00\",\"mainEntityOfPage\":{\"@id\":\"https:\\\/\\\/www.marketnewsdesk.com\\\/index.php\\\/anavex-life-sciences-highlights-new-scientific-findings-on-shared-biology-between-autism-and-alzheimers-disease\\\/\"},\"wordCount\":2355,\"image\":{\"@id\":\"https:\\\/\\\/www.marketnewsdesk.com\\\/index.php\\\/anavex-life-sciences-highlights-new-scientific-findings-on-shared-biology-between-autism-and-alzheimers-disease\\\/#primaryimage\"},\"thumbnailUrl\":\"https:\\\/\\\/www.globenewswire.com\\\/newsroom\\\/ti?nf=OTY4OTAwMCM3NTMzMzc5IzIwMTk1Mzk=\",\"inLanguage\":\"en-US\"},{\"@type\":\"WebPage\",\"@id\":\"https:\\\/\\\/www.marketnewsdesk.com\\\/index.php\\\/anavex-life-sciences-highlights-new-scientific-findings-on-shared-biology-between-autism-and-alzheimers-disease\\\/\",\"url\":\"https:\\\/\\\/www.marketnewsdesk.com\\\/index.php\\\/anavex-life-sciences-highlights-new-scientific-findings-on-shared-biology-between-autism-and-alzheimers-disease\\\/\",\"name\":\"Anavex Life Sciences Highlights New Scientific Findings on Shared Biology Between Autism and Alzheimer\u2019s Disease - 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