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Pathophysiology and Neuroimmune Interactions Underlying Parkinson's Disease and Traumatic Brain Injury.
Lillian, Alyssa; Zuo, Wanhong; Laham, Linda; Hilfiker, Sabine; Ye, Jiang-Hong.
Afiliación
  • Lillian A; New Jersey Medical School, Rutgers University, 185 South Orange Avenue, Newark, NJ 08901, USA.
  • Zuo W; New Jersey Medical School, Rutgers University, 185 South Orange Avenue, Newark, NJ 08901, USA.
  • Laham L; New Jersey Medical School, Rutgers University, 185 South Orange Avenue, Newark, NJ 08901, USA.
  • Hilfiker S; New Jersey Medical School, Rutgers University, 185 South Orange Avenue, Newark, NJ 08901, USA.
  • Ye JH; Department of Anesthesiology, Pharmacology, Physiology & Neuroscience, New Jersey Medical School, Rutgers University, 185 South Orange Avenue, Newark, NJ 08901, USA.
Int J Mol Sci ; 24(8)2023 Apr 13.
Article en En | MEDLINE | ID: mdl-37108349
Parkinson's disease (PD) is a progressive neurodegenerative disorder clinically defined by motor instability, bradykinesia, and resting tremors. The clinical symptomatology is seen alongside pathologic changes, most notably the loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc) and the accumulation of α-synuclein and neuromelanin aggregates throughout numerous neural circuits. Traumatic brain injury (TBI) has been implicated as a risk factor for developing various neurodegenerative diseases, with the most compelling argument for the development of PD. Dopaminergic abnormalities, the accumulation of α-synuclein, and disruptions in neural homeostatic mechanisms, including but not limited to the release of pro-inflammatory mediators and the production of reactive oxygen species (ROS), are all present following TBI and are closely related to the pathologic changes seen in PD. Neuronal iron accumulation is discernable in degenerative and injured brain states, as is aquaporin-4 (APQ4). APQ4 is an essential mediator of synaptic plasticity in PD and regulates edematous states in the brain after TBI. Whether the cellular and parenchymal changes seen post-TBI directly cause neurodegenerative diseases such as PD is a point of considerable interest and debate; this review explores the vast array of neuroimmunological interactions and subsequent analogous changes that occur in TBI and PD. There is significant interest in exploring the validity of the relationship between TBI and PD, which is a focus of this review.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Enfermedad de Parkinson / Enfermedades Neurodegenerativas / Lesiones Traumáticas del Encéfalo Tipo de estudio: Risk_factors_studies Límite: Humans Idioma: En Revista: Int J Mol Sci Año: 2023 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Suiza
Texto completo
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XML
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Enfermedad de Parkinson / Enfermedades Neurodegenerativas / Lesiones Traumáticas del Encéfalo Tipo de estudio: Risk_factors_studies Límite: Humans Idioma: En Revista: Int J Mol Sci Año: 2023 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Suiza