Sudden infant death syndrome: Postulated role of impaired vasoactive neuropeptide-related inflammatory modulation

摘要: Sudden infant death syndrome (SIDS) has been extensively investigated in the context of infection as a contributing factor otherwise apparently healthy infants. A number infectious agents have implicated suggesting causal pathomechanism is related to infection, but not necessarily solely attributable any one type infection. An alternative provocative hypothesis that post-infection autoimmunity affecting critical novel neurotransmitters vasoactive neuropeptide family. Their role respiratory and cardiac functioning together with hypotheses postulating their autoimmune compromise may suggest SIDS etiology following Animal models demonstrate vital neonatal survival neuronal control breathing. Autoimmune receptors through molecular mimicry or idiopathic postulated cause SIDS.