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<p>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.</p>

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Common molecular signatures: the role of BDNF, melatonin, and orexin in the ASD-schizophrenia continuum

  • 期刊论文

  • 发表日期：

    2026年4月17日

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  • Nahi Sabih Alruwaili,
  • Hayder M. Al-Kuraishy,
  • Ali I. Al-Gareeb,
  • Mustafa M. Shokr,
  • Neda M. Bogari,
  • Suhair Alhelfawi,
  • Mubarak Alruwaili,
  • Gaber El-Saber Batiha

摘要

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.