ArticleForensic science, medicine, and pathology2018
Neuronal apoptosis in the brainstem medulla of sudden unexpected death in infancy (SUDI), and the importance of standardized SUDI classification.
Article in Forensic science, medicine, and pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- A narrative review of sudden infant death syndrome: pathophysiology, risk factors, and prevention.European journal of pediatrics · 2026Review
- Forensic neuropathology in the past decade: a scoping literature review.Forensic science, medicine, and pathology · 2024Article
- Cell death in the lateral geniculate nucleus, and its possible relationship with nicotinic receptors and sudden infant death syndrome (SIDS).Molecular neurobiology · 2023Article
- Article
- Individual variability in the size and organization of the human arcuate nucleus of the medulla.Brain structure & function · 2022Article
- The Unfolded Protein Response in the Human Infant Brain and Dysregulation Seen in Sudden Infant Death Syndrome (SIDS).Molecular neurobiology · 2021Article
- Nitric oxide controls excitatory/inhibitory balance in the hypoglossal nucleus during early postnatal development.Brain structure & function · 2020Article
- Microglia in the human infant brain and factors that affect expression.Brain, behavior, & immunity - health · 2020Article
- Cell death in the human infant central nervous system and in sudden infant death syndrome (SIDS).Apoptosis : an international journal on programmed cell death · 2019Article
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The purpose of this study was to examine the neuronal expression of apoptotic markers in the rostral medulla of a newly characterized dataset of sudden unexpected death in infancy (SUDI), and to determine the impact of diagnostic groupings on these findings and whether they pertain to the intrinsic apoptotic pathway. Immunohistochemical staining was quantified to determine the percentage of neurons positive for active caspase-9 (specific to the intrinsic apoptotic pathway), active caspase-3 (common to the intrinsic and extrinsic apoptotic pathways) and Terminal deoxynucleotidyl transferase mediated dUTP nick-end labelling (TUNEL) (labels DNA fragmentation) in nine nuclei of the rostral medulla. Expression was compared between groups of SUDI infants where the cause of death was initially classified by a forensic pathologist or subsequently after reclassification by an expert panel using the San Diego Criteria. 68 SUDI infants were studied and originally classified as explained SUDI (n = 12), Sudden Infant Death Syndrome (SIDS) (n = 27) and undetermined (n = 29). Reclassification resulted in a decrease in the number of explained SUDI cases to 7 and a decrease in the number of undetermined cases to 4, with a corresponding increase in the number of SIDS cases to 57 (8 SIDS I; 49 SIDS II). The expression of apoptotic markers was similar in explained SUDI and SIDS I infants. However, TUNEL expression was greater in the cuneate (p < 0.001), vestibular (p = 0.01) and hypoglossal (p < 0.001) nuclei and active caspase-3 expression was lower in the arcuate nucleus (p = 0.037) in SIDS II compared to explained Sudden Unexpected Death in Infancy (eSUDI) infants. Compared to SIDS I infants, SIDS II infants had greater TUNEL expression in the dorsal motor nucleus of the vagus (p < 0.01) and greater active caspase-9 expression in the medial and spinal vestibular nuclei (p = <0.01). Changes in apoptotic expression predominated in SIDS II infants. We postulate that these are due to a combination of contributing risk factors including the presence of an upper respiratory tract infection and bed-sharing/co-sleeping. The absence of changes in active caspase-9 expression compared to eSUDI indicates that the intrinsic apoptotic pathway is not upregulated in SIDS.
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