{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,9]],"date-time":"2026-09-09T11:19:50Z","timestamp":1788952790303,"version":"build-2803163510"},"reference-count":153,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,9,9]],"date-time":"2026-09-09T00:00:00Z","timestamp":1788912000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Mol. Neurosci."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Autism spectrum disorder (ASD) is a neurodevelopmental condition characterized by social communication differences and restricted, repetitive behaviors. Convergent evidence implicates prefrontal cortex (PFC) circuit dysregulation and chronic neuroimmune activation in ASD. Despite increasing off-label use of guanfacine in children and adolescents with autism, its molecular and immunological rationale remains incompletely synthesized.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>To synthesize current evidence regarding the molecular, neurophysiological, and immunological mechanisms through which guanfacine may influence ASD-related neural and immune dysfunction.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>In this narrative review, we integrated evidence from pharmacology, systems neuroscience, immunology, and clinical studies to examine two converging mechanisms by which guanfacine may act in ASD and related conditions.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Guanfacine suppresses cAMP signaling through \u03b12A-adrenoceptor activation, producing dual neuronal and immune effects. In PFC pyramidal neurons, reduced cAMP signaling promotes closure of hyperpolarization-activated cyclic nucleotide-gated (HCN) channels, strengthening network firing that supports working memory, attention, and emotion regulation. In parallel, activation of \u03b12A-adrenoceptors on microglia and macrophages reduces production of pro-inflammatory cytokines, including tumor necrosis factor-\u03b1, interleukin-1\u03b2, and interleukin-6, while promoting anti-inflammatory phenotypes through nuclear factor kappa B suppression and peroxisome proliferator-activated receptor gamma activation. Evidence from human studies and ASD models indicates that \u03b12A-adrenoceptor signaling, HCN channel function, and microglial reactivity are altered in autism and converge on synaptic refinement, dendritic spine stability, and PFC-dependent behavior. We further review clinical evidence for guanfacine in individuals with autism and in related conditions, including attention-deficit\/hyperactivity disorder, post-traumatic stress disorder, traumatic brain injury, post-COVID cognitive impairment, delirium, and age-related cognitive decline.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Collectively, the available evidence supports a mechanistic framework linking guanfacine, HCN channel modulation, and neuroimmune regulation, thereby bridging neuroinflammation and PFC function in ASD. The broader \u03b12A\u2013HCN\u2013microglia axis may represent a promising therapeutic target for PFC- and neuroimmune-related features of ASD; however, adequately powered autism-specific randomized trials and biomarker-informed stratification strategies are needed to establish clinical efficacy and validate this framework.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fnmol.2026.1915506","type":"journal-article","created":{"date-parts":[[2026,9,9]],"date-time":"2026-09-09T11:02:51Z","timestamp":1788951771000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Guanfacine and HCN channels: bridging neuroinflammation and prefrontal cortex function in autism spectrum disorder"],"prefix":"10.3389","volume":"19","author":[{"given":"Kazuhiko","family":"Yamamuro","sequence":"first","affiliation":[{"name":"Center for Health Control, Nara Medical University, Kashihara","place":["Nara, Japan"]},{"name":"Department of Psychiatry, Nara Medical University, Kashihara","place":["Nara, Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Takahira","family":"Yamauchi","sequence":"additional","affiliation":[{"name":"Department of Psychiatry, Nara Medical University, Kashihara","place":["Nara, Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Manabu","family":"Makinodan","sequence":"additional","affiliation":[{"name":"Department of Neuropsychiatry, Kumamoto University","place":["Kumamoto, Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,9,9]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"547","DOI":"10.1016\/j.ebiom.2018.10.021","article-title":"Surgery, neuroinflammation and cognitive impairment.","volume":"37","author":"Alam","year":"2018","journal-title":"EBiomedicine"},{"key":"B2","doi-asserted-by":"publisher","first-page":"181","DOI":"10.1016\/0006-8993(94)91782-5","article-title":"Perikaryal and synaptic localization of \u03b12A-adrenergic receptor-like immunoreactivity.","volume":"650","author":"Aoki","year":"1994","journal-title":"Brain Res."},{"key":"B3","doi-asserted-by":"publisher","first-page":"229","DOI":"10.1113\/jphysiol.2005.104042","article-title":"Hyperpolarization-activated cation channels in fast-spiking interneurons of rat hippocampus.","volume":"574","author":"Aponte","year":"2006","journal-title":"J. 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