ArticleJournal of cellular physiology2015
Alpha-synuclein as a pathological link between chronic traumatic brain injury and Parkinson's disease.
Article in Journal of cellular physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers.
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Who cites it
105 citing papers in PubMed, 152 citations in OpenAlex.
- Traumatic Brain Injury and the Road to Alzheimer's Disease.Biomedicines · 2026Review
- Neuroimmune interactions: from molecular mechanisms to therapeutic targets.Molecular biomedicine · 2026Review
- Tau catalyzes amyloid-β aggregation and toxicity in a polymorph-dependent manner.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- PERK Deficiency Amplifies Molecular, Structural, and Network Vulnerability to Repetitive Mild Traumatic Brain Injury.bioRxiv : the preprint server for biology · 2026Article
- Posterior fossa arachnoid cysts in multiple system atrophy.IBRO neuroscience reports · 2025Article
- Lasting Impact: Exploring the Brain Mechanisms that Link Traumatic Brain Injury to Parkinson's Disease.Molecular neurobiology · 2025Review
- Cellular and molecular mechanisms of pathological tau phosphorylation in traumatic brain injury: implications for chronic traumatic encephalopathy.Molecular neurodegeneration · 2025Review
- Advantages and challenges of using allogeneic vs. autologous sources for neuronal cell replacement in Parkinson's disease: Insights from non-human primate studies.Brain research bulletin · 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
- Does white matter and vascular injury from repetitive head impacts lead to a novel pattern on T2 FLAIR MRI? A hypothesis proposal and call for research.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- Adolescent mice exposed to TBI developed PD-like pathology in middle age.Translational psychiatry · 2025Article
- Non-invasive therapeutics for neurotrauma: a mechanistic overview.Frontiers in neurology · 2025Review
- Assessment of Neurobehavioral Performance and Markers of Synaptic Vesicle Trafficking in an Alpha-Synuclein Knockout Mouse Model after Controlled Cortical Impact Injury.Neurotrauma reports · 2025Article
- The Relevance and Implications of Monoclonal Antibody Therapies on Traumatic Brain Injury Pathologies.Biomedicines · 2024Review
- The Role of α-Synuclein in Etiology of Neurodegenerative Diseases.International journal of molecular sciences · 2024Review
- An antioxidant and anti-ER stress combination therapy elevates phosphorylation of α-Syn at serine 129 and alleviates post-TBI PD-like pathology in a sex-specific manner in mice.Experimental neurology · 2024Article
- Epidemiology of Parkinson's Disease: An Update.Current neurology and neuroscience reports · 2024Review
- The contribution of β-amyloid, Tau and α-synuclein to blood-brain barrier damage in neurodegenerative disorders.Acta neuropathologica · 2024Review
- Dysregulation of the dopaminergic system secondary to traumatic brain injury: implications for mood and anxiety disorders.Frontiers in neuroscience · 2024Review
- American Football Play and Parkinson Disease Among Men.JAMA network open · 2023Article
45 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The long-term consequences of traumatic brain injury (TBI) are closely associated with the development of histopathological deficits. Notably, TBI may predispose long-term survivors to age-related neurodegenerative diseases, such as Parkinson's disease (PD), which is characterized by a gradual degeneration of the nigrostriatal dopaminergic neurons. However, preclinical studies on the pathophysiological changes in substantia nigra (SN) after chronic TBI are lacking. In the present in vivo study, we examined the pathological link between PD-associated dopaminergic neuronal loss and chronic TBI. Sixty days post-TBI, rats were euthanized and brain tissues harvested. Immunostaining was performed using tyrosine hydroxylase (TH), an enzyme required for the synthesis of dopamine in neurons, α-synuclein, a presynaptic protein that plays a role in synaptic vesicle recycling, and major histocompatibility complex II (MHCII), a protein found in antigen presenting cells such as inflammatory microglia cells, all key players in PD pathology. Unbiased stereology analyses revealed significant decrease of TH-positive expression in the surviving dopaminergic neurons of the SN pars compacta (SNpc) relative to sham control. In parallel, increased α-synuclein accumulation was detected in the ipsilateral SN compared to the contralateral SN in TBI animals or sham control. In addition, exacerbation of MHCII+ cells was recognized in the SN and cerebral peduncle ipsilateral to injury relative to contralateral side and sham control. These results suggest α-synuclein as a pathological link between chronic effects of TBI and PD symptoms as evidenced by significant overexpression and abnormal accumulation of α-synuclein in inflammation-infiltrated SN of rats exposed to chronic TBI.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.