ReviewMolecular biology reports2026
Common molecular signatures: the role of BDNF, melatonin, and orexin in the ASD-schizophrenia continuum.
Review in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
8 authors.
Funding
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Abstract
Autism spectrum disorder (ASD) and schizophrenia share overlapping neurobiological mechanisms, including dysregulation of dopamine, serotonin, glutamate, acetylcholine, and gamma-aminobutyric acid (GABA) neurotransmission, as well as alterations in brain-derived neurotrophic factor (BDNF) and neuromodulators (melatonin, orexin). Both disorders exhibit genetic and structural brain abnormalities, contributing to social and cognitive deficits. ASD is characterized by repetitive behaviors and social impairments, while schizophrenia presents with positive (hallucinations) and negative (social withdrawal) symptoms, yet both involve disrupted excitatory/inhibitory balance. Dopaminergic hyperactivity in schizophrenia contrasts with ASD’s prefrontal dopamine deficiency, while serotonin dysregulation is common to both. Glutamate hypofunction in schizophrenia differs from ASD’s variable N-methyl-D-aspartate receptor (NMDA) receptor dysfunction, yet memantine shows therapeutic potential in both: cholinergic deficits and GABAergic impairment further link these disorders. Neuroinflammatory and epigenetic mechanisms, including microRNA dysregulation and BDNF alterations, exacerbate synaptic dysfunction. Clinically, antipsychotics (e.g., risperidone) and serotonin modulators improve symptoms in both conditions, while melatonin ameliorates sleep disturbances. Emerging therapies targeting shared pathways, including NMDA modulators and orexin antagonists, hold promise. Despite preclinical evidence, translational gaps remain due to heterogeneous clinical presentations. This review highlights the mechanistic convergence of ASD and schizophrenia, advocating for integrated treatment strategies and further research into comorbid pathophysiology to refine diagnostic and therapeutic approaches.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.