Hypothermia Shifts Neurodegeneration Phenotype in Neonatal Human Hypoxic-Ischemic Encephalopathy but Not in Related Piglet Models: Possible Relationship to Toxic Conformer and Intrinsically Disordered Prion-like Protein Accumulation.
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ABSTRACT: Hypothermia (HT) is used clinically for neonatal hypoxic-ischemic encephalopathy (HIE); however, the brain protection is incomplete and selective regional vulnerability and lifelong consequences remain. Refractory damage and impairment with HT cooling/rewarming could result from unchecked or altered persisting cell death and proteinopathy. We tested two hypotheses: (1) HT modifies neurodegeneration type, and (2) intrinsically disordered proteins (IDPs) and encephalopathy cause toxic conformer protein (TCP) proteinopathy neonatally. We studied postmortem human neonatal HIE cases with or without therapeutic HT, neonatal piglets subjected to global hypoxia-ischemia (HI) with and without HT or combinations of HI and quinolinic acid (QA) excitotoxicity surviving for 29-96 h to 14 days, and huma
SUBMITTER: Martin LJ
PROVIDER: S-EPMC12025496 | biostudies-literature | 2025 Apr
REPOSITORIES: biostudies-literature
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