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Background <p>Sudden infant death syndrome (SIDS) occurs predominantly during sleep between 2 and 6 months of age, suggesting impaired maturation of arousal pathways. The neurobiological mechanisms involved remain unclear. We investigated the role of wake-promoting Orexin (Ox) and Histamine (HA) neurons in SIDS.</p> Methods <p>Cerebrospinal fluid (CSF) Ox levels were measured in 61 living controls and 70 Sudden Unexpected Death Infants (SUDI: 38 SIDS, 32 explained deaths (ED)). HA and tele-methylhistamine (t-MeHA) were analyzed in an additional 46 SUDI (34 SIDS, 12 ED) and 42 controls. Immunohistochemistry was performed on hypothalamic tissue from 11 SIDS and 8 ED cases to quantify Ox and HA neuron numbers.</p> Results <p>CSF Ox levels did not differ overall between groups but were higher in SUDI infants aged 2–6 months. HA and t-MeHA levels were elevated in SUDI, likely reflecting postmortem release. Ox neuron numbers were increased in rostral hypothalamic region in SIDS compared with EDs, whereas HA neuron numbers were unchanged.</p> Conclusions <p>SIDS is associated with increased Ox neuronal activity during the peak risk period, possibly reflecting a homeostatic upregulation in response to arousal deficit or repeated stress or hypoxia, while the role&#xa0;of&#xa0;HA system remains to be clarified with more sensitive biomarkers.</p> Impact <p><UnorderedList Mark="Bullet"> <ItemContent> <p>First study evaluating orexin and histamine systems in SIDS using CSF and postmortem brain tissue.</p> </ItemContent> <ItemContent> <p>Identifies elevated orexin activity in SIDS infants, particularly in the 2–6 month risk window.</p> </ItemContent> <ItemContent> <p>No evidence to date for direct histamine involvement; need for more sensitive biomarkers.</p> </ItemContent> <ItemContent> <p>Suggests orexin system as a potential biomarker for SIDS risk stratification.</p> </ItemContent> <ItemContent> <p>Highlights the importance of combined neurobiological approaches for prevention.</p> </ItemContent> </UnorderedList></p>

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A quest for a histaminergic or orexinergic biomarker for sudden infant death syndrome

  • 期刊论文

  • 发表日期：

    2026年6月22日

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  • Yan Zhao,
  • Guang-Fu Cui,
  • Sabine Plancoulaine,
  • Marion Comajuan,
  • Marine Bersault,
  • Clara Inocente,
  • Yi-Ping Hou,
  • Yves Dauvilliers,
  • Manuela Lotierzo,
  • Aurore Guyon,
  • David Meyronet,
  • Anne Jouvet,
  • Beatrice Kugener,
  • Marine Thieux,
  • Philippe Robert,
  • Jian-Sheng Lin,
  • Patricia Franco

摘要

Background

Sudden infant death syndrome (SIDS) occurs predominantly during sleep between 2 and 6 months of age, suggesting impaired maturation of arousal pathways. The neurobiological mechanisms involved remain unclear. We investigated the role of wake-promoting Orexin (Ox) and Histamine (HA) neurons in SIDS.

Methods

Cerebrospinal fluid (CSF) Ox levels were measured in 61 living controls and 70 Sudden Unexpected Death Infants (SUDI: 38 SIDS, 32 explained deaths (ED)). HA and tele-methylhistamine (t-MeHA) were analyzed in an additional 46 SUDI (34 SIDS, 12 ED) and 42 controls. Immunohistochemistry was performed on hypothalamic tissue from 11 SIDS and 8 ED cases to quantify Ox and HA neuron numbers.

Results

CSF Ox levels did not differ overall between groups but were higher in SUDI infants aged 2–6 months. HA and t-MeHA levels were elevated in SUDI, likely reflecting postmortem release. Ox neuron numbers were increased in rostral hypothalamic region in SIDS compared with EDs, whereas HA neuron numbers were unchanged.

Conclusions

SIDS is associated with increased Ox neuronal activity during the peak risk period, possibly reflecting a homeostatic upregulation in response to arousal deficit or repeated stress or hypoxia, while the role of HA system remains to be clarified with more sensitive biomarkers.

Impact

First study evaluating orexin and histamine systems in SIDS using CSF and postmortem brain tissue.

Identifies elevated orexin activity in SIDS infants, particularly in the 2–6 month risk window.

No evidence to date for direct histamine involvement; need for more sensitive biomarkers.

Suggests orexin system as a potential biomarker for SIDS risk stratification.

Highlights the importance of combined neurobiological approaches for prevention.