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Traumatic Brain Injury Leads to Later Development of Parkinson's Disease in Mice
Author(s) -
Impellizzeri Daniela,
Bruschetta Giuseppe,
Cordaro Marika,
Crupi Rosalia,
Cuzzocrea Salvatore,
Esposito Emanuela
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.771.1
Subject(s) - traumatic brain injury , substantia nigra , dopamine transporter , neuroinflammation , medicine , dopaminergic , tyrosine hydroxylase , glial cell line derived neurotrophic factor , neurotrophic factors , parkinson's disease , neuroscience , dopamine , disease , psychology , psychiatry , receptor
Central nervous insults, such as traumatic brain injury (TBI), are among the leading causes of mortality and morbidity worldwide. TBI is an insult to the brain from the application of external physical force that leads to temporary or permanent structural and functional impairment of the brain. Traumatic brain injuries are reported as risk factors for sporadic neurodegenerative diseases. Parkinson's disease (PD) is a late‐onset neurodegenerative disorder caused by degeneration of dopaminergic neurons in the substantia nigra (SNc). In that regard, the aim of this study was to investigate the possible development of PD following experimental model of TBI. Specifically, TBI was induced in mice by controlled cortical impactor. At different time points behavioral tests (Open field and Elevated plus maze tests) were performed; the animals were sacrificed 30 days after TBI and the brains were collected.Our results showed that following TBI there was decreased expression of tyrosine hydroxylase (TH) and dopamine transporter (DAT) in the SNc, which are specific markers of PD, and significant behavioral alterations. In addition, a strong increase in neuroinflammation evaluated as GFAP, TNF‐α, COX‐2, iNOS expressions, IκB‐α degradation, and NF‐κB translocation, was evident. Interestingly, neurotrophic factors such as BDNF, NT3, NGF, GDNF were also decreased after TBI ‐induced PD at 30 days after TBI. In conclusion, in this study, we suggested that there are currently under‐appreciated biological mechanisms linking brain injury and neurodegenerative diseases.