ArticleCNS neuroscience & therapeutics2024
Neonatal stress disrupts the glymphatic system development and increases the susceptibility to Parkinson's disease in later life.
Article in CNS neuroscience & therapeutics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- WWOX Mutation as a Rare Cause of Neonatal-Infantile Parkinsonism Mimicking a Neurotransmitter Disorder: A Case Report.Journal of paediatrics and child health · 2026Article
- Perivascular spread of CSF-derived α-synuclein oligomers drives region-specific Parkinson's-like pathology.NPJ Parkinson's disease · 2026Article
- Glymphatic-meningeal lymphatic system imbalance: a peripheral-to-central inflammatory bridge in perioperative neurocognitive disorders.Frontiers in immunology · 2026Review
- Perceiving traumatic brain injury from glymphatic system.Molecular psychiatry · 2025Review
- The glymphatic and meningeal lymphatic systems may converge, connecting traumatic brain injury progression with chronic traumatic encephalopathy onset.Molecular and cellular neurosciences · 2025Review
- Development of perivascular astrocyte processes.Frontiers in neuroscience · 2025Review
- Neonatal stress disrupts the glymphatic system development and increases the susceptibility to Parkinson's disease in later life.CNS neuroscience & therapeutics · 2024Article
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Authors and funding
8 authors.
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Abstract
introductionNeonatal stress disrupts brain development and increases the risk of neurological disorders later in life. However, the impact of neonatal stress on the development of the glymphatic system and susceptibility to Parkinson's disease (PD) remains largely unknown.
methodsNeonatal maternal deprivation (NMD) was performed on mice for 14 consecutive days to model chronic neonatal stress. Adeno-associated virus expressing A53T-α-synuclein (α-syn) was injected into the substantia nigra to establish PD model mice. Glymphatic activity was determined using in vivo magnetic resonance imaging, ex vivo fluorescence imaging and microplate assay. The transcription and expression of aquaporin-4 (AQP4) and other molecules were evaluated by qPCR, western blotting, and immunofluorescence. Animal's responses to NMD and α-syn overexpression were observed using behavioral tests.
resultsGlymphatic activity was impaired in adult NMD mice. AQP4 polarization and platelet-derived growth factor B (PDGF-B) signaling were reduced in the frontal cortex and hippocampus of both young and adult NMD mice. Furthermore, exogenous α-syn accumulation was increased and PD-like symptoms were aggravated in adult NMD mice.
conclusionThe results demonstrated that NMD could disrupt the development of the glymphatic system through PDGF-B signaling and increase the risk of PD later in life, indicating that alleviating neonatal stress could be beneficial in protecting the glymphatic system and reducing susceptibility to neurodegeneration.
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