ArticleMolecular and cellular neurosciences2019
Acrolein-mediated alpha-synuclein pathology involvement in the early post-injury pathogenesis of mild blast-induced Parkinsonian neurodegeneration.
Article in Molecular and cellular neurosciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 38 citations in OpenAlex.
- Reactive aldehyde species-mediated neuropathic pain in spinal cord injury: Mechanisms and therapeutic opportunities.Neural regeneration research · 2026Article
- Lipid peroxidation in cancer: a double-edged sword shaping progression and therapy.Medical oncology (Northwood, London, England) · 2026Review
- Proteomic analysis reveals shared biological pathways linking acrolein to biomolecular changes in the acute phase of rat spinal cord injury.bioRxiv : the preprint server for biology · 2026Article
- Acrolein-Induced Alterations in Morphology and Stress Resilience in hiPSC-Derived Cortical Neurons.Environmental science & technology · 2025Article
- Concussive injuries induce neuronal stress-dependent tau mislocalization to dendritic spines with acrolein and functional network alteration in TBI-on-a-chip.Lab on a chip · 2025Article
- Impact Induces Phagocytic Defect in Reactive Microglia.bioRxiv : the preprint server for biology · 2025Article
- Lasting Impact: Exploring the Brain Mechanisms that Link Traumatic Brain Injury to Parkinson's Disease.Molecular neurobiology · 2025Review
- History of Traumatic Brain Injury Does Not Influence Rate of Progression of Clinical or Pathological Outcomes in Two Early Parkinson's Disease Cohorts.European journal of neurology · 2025Observational
- Adolescent mice exposed to TBI developed PD-like pathology in middle age.Translational psychiatry · 2025Article
- Oxidative Stress-mediated Lipid Peroxidation-derived Lipid Aldehydes in the Pathophysiology of Neurodegenerative Diseases.Current neuropharmacology · 2025Review
- Temporal differential effects of post-injury alcohol consumption in a mouse model of blast-induced traumatic brain injury.Neuroscience · 2024Article
- Physical Exercise-Induced Activation of NRF2 and BDNF as a Promising Strategy for Ferroptosis Regulation in Parkinson's Disease.Neurochemical research · 2024Review
- Modulation of TRPV1 and TRPA1 Channels Function by Sea Anemones' Peptides Enhances the Viability of SH-SY5Y Cell Model of Parkinson's Disease.International journal of molecular sciences · 2023Article
- Traumatic brain injury-associated epigenetic changes and the risk for neurodegenerative diseases.Frontiers in neuroscience · 2023Article
- Oxidative stress-induced phosphorylation of JIP4 regulates lysosomal positioning in coordination with TRPML1 and ALG2.The EMBO journal · 2022Article
- The Role of Acrolein in Neurodegenerative Diseases and Its Protective Strategy.Foods (Basel, Switzerland) · 2022Review
- Utilizing novel TBI-on-a-chip device to link physical impacts to neurodegeneration and decipher primary and secondary injury mechanisms.Scientific reports · 2022Article
- Origin and Fate of Acrolein in Foods.Foods (Basel, Switzerland) · 2022Review
- Critical role of mitochondrial aldehyde dehydrogenase 2 in acrolein sequestering in rat spinal cord injury.Neural regeneration research · 2022Article
- Olfactory Bulb Excitotoxicity as a Gap-Filling Mechanism Underlying the Link Between Traumatic Brain Injury-Induced Secondary Neuronal Degeneration and Parkinson's Disease-Like Pathology.Neurochemical research · 2022Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Survivors of blast-induced traumatic brain injury (bTBI) have increased susceptibility to Parkinson's disease (PD), characterized by α-synuclein aggregation and the progressive degeneration of nigrostriatal dopaminergic neurons. Using an established bTBI rat model, we evaluated the changes of α-synuclein and tyrosine hydroxylase (TH), known hallmarks of PD, and acrolein, a reactive aldehyde and marker of oxidative stress, with the aim of revealing key pathways leading to PD post-bTBI. Indicated in both animal models of PD and TBI, acrolein is likely a point of pathogenic convergence. Here we show that after a single mild bTBI, acrolein is elevated up to a week, systemically in urine, and in whole brain tissue, specifically the substantia nigra and striatum. Acrolein elevation is accompanied by heightened α-synuclein oligomerization, dopaminergic dysregulation, and acrolein/α-synuclein interaction in the same brain regions. We further show that acrolein can directly modify and oligomerize α-synuclein in vitro. Taken together, our data suggests acrolein likely plays an important role in inducing PD pathology following bTBI by encouraging α-synuclein aggregation. These results are expected to advance our understanding of the long-term post-bTBI pathological changes leading to the development of PD, and suggest intervention targets to curtail such pathology.
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