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<p>Preeclampsia is a hypertensive disorder of pregnancy that has emerged as a significant prenatal risk factor for autism spectrum disorder (ASD) in offspring. Accumulating epidemiological and experimental evidence suggests that placental dysfunction, systemic inflammation, oxidative stress, and impaired cellular autophagy in preeclampsia contribute to fetal neurodevelopmental disturbances. This review elucidates the shared molecular pathways between preeclampsia and ASD, including over-activation of inflammatory signaling, dysregulation of placental growth factor (PlGF), and disturbances in autophagy. Genetic overlaps between preeclampsia and ASD further strengthen the biological plausibility of this association. These findings support the hypothesis that early-onset preeclampsia induces a neuroinflammatory and hypoxic intrauterine environment that adversely programs the fetal brain, potentially leading to ASD. Understanding of these mechanisms may open new preventive strategies targeting placental health and maternal immune modulation during pregnancy to mitigate ASD risk.</p>

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Placental dysfunction, inflammation, and impaired autophagy in preeclampsia: A pathophysiological link to autism spectrum disorder

  • 期刊论文

  • 发表日期：

    2026年4月16日

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  • Anass M. Abbas,
  • Hayder M. Al-kuraishy,
  • Al-Maiahy. Thabat J,
  • Ali I. Al-Gareeb,
  • Aya M. Mustafa,
  • Athanasios Alexiou,
  • Marios Papadakis,
  • Gaber El-Saber Batiha

摘要

Preeclampsia is a hypertensive disorder of pregnancy that has emerged as a significant prenatal risk factor for autism spectrum disorder (ASD) in offspring. Accumulating epidemiological and experimental evidence suggests that placental dysfunction, systemic inflammation, oxidative stress, and impaired cellular autophagy in preeclampsia contribute to fetal neurodevelopmental disturbances. This review elucidates the shared molecular pathways between preeclampsia and ASD, including over-activation of inflammatory signaling, dysregulation of placental growth factor (PlGF), and disturbances in autophagy. Genetic overlaps between preeclampsia and ASD further strengthen the biological plausibility of this association. These findings support the hypothesis that early-onset preeclampsia induces a neuroinflammatory and hypoxic intrauterine environment that adversely programs the fetal brain, potentially leading to ASD. Understanding of these mechanisms may open new preventive strategies targeting placental health and maternal immune modulation during pregnancy to mitigate ASD risk.