ReviewFrontiers in pediatrics2025
Perinatal asphyxia and Alzheimer's disease: is there a correlation?
Review in Frontiers in pediatrics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed.
- Nipah virus infects the brain and triggers neuronal and glial damage in a hamster model.Journal of neuroinflammation · 2026Article
- Microglial Activation Under Hypoxic Conditions in Early Alzheimer's Disease: Can Natural SIRT1 Activators Be Therapeutic Allies in the Inflammation-Energy Axis?Phytotherapy research : PTR · 2026Review
- Alterations of Apolipoprotein A1, E, and J Genes in the Frontal Cortex in an Ischemic Model of Alzheimer's Disease with 2-Year Survival.International journal of molecular sciences · 2025Article
- New Generation of Clinical Epigenetics Analysis and Diagnosis for Precision Medicine.Diagnostics (Basel, Switzerland) · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The perinatal development period is critical for the formation of brain structures responsible for cognitive functions. Disruptions during this phase, such as perinatal asphyxia, characterized by impaired gas exchange and hypoxia, can lead to long-lasting neuronal damage and increased susceptibility to neurodegenerative diseases, including Alzheimer's disease (AD). AD, the most common cause of dementia globally, is marked by amyloid plaques, neurofibrillary tangles, and progressive cognitive decline. Emerging evidence links perinatal asphyxia with an elevated risk of AD, highlighting the potential role of oxidative stress, neuroinflammation, and epigenetic modifications as mediators. This review explores the mechanisms underlying brain damage after perinatal asphyxia, emphasizing oxidative stress, inflammation, and epigenetic changes that contribute to lifelong neurodegenerative susceptibility. Additionally, biomarkers identified in animal models reveal parallels between perinatal asphyxia and AD pathology, such as amyloid precursor protein alterations, gliosis, and microglial activation. These findings suggest perinatal asphyxia may prime microglia and epigenetically alter gene expression, predisposing individuals to chronic neurodegeneration. Future research should leverage advanced methodologies, including transcriptomics, epigenomics, and aged brain organoid models, to elucidate early-life influences on AD development. Understanding these mechanisms may pave the way for novel prevention strategies targeting early-life risk factors for neurodegenerative diseases.
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Registered trials
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