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Parkinson's disease: Autoimmunity and neuroinflammation.
Autoimmun Rev. 2016 Oct; 15(10):1005-11.AR

Abstract

Parkinson's disease is a neurodegenerative disease that causes the death of dopaminergic neurons in the substantia nigra. The resulting dopamine deficiency in the basal ganglia leads to a movement disorder that is characterized by classical parkinsonian motor symptoms. Parkinson's disease is recognized as the most common neurodegenerative disorder after Alzheimer's disease. PD ethiopathogenesis remains to be elucidated and has been connected to genetic, environmental and immunologic conditions. The past decade has provided evidence for a significant role of the immune system in PD pathogenesis, either through inflammation or an autoimmune response. Several autoantibodies directed at antigens associated with PD pathogenesis have been identified in PD patients. This immune activation may be the cause of, rather than a response to, the observed neuronal loss. Parkinsonian motor symptoms include bradykinesia, muscular rigidity and resting tremor. The non-motor features include olfactory dysfunction, cognitive impairment, psychiatric symptoms and autonomic dysfunction. Microscopically, the specific degeneration of dopaminergic neurons in the substantia nigra and the presence of Lewy bodies, which are brain deposits containing a substantial amount of α-synuclein, have been recognized. The progression of Parkinson's disease is characterized by a worsening of motor features; however, as the disease progresses, there is an emergence of complications related to long-term symptomatic treatment. The available therapies for Parkinson's disease only treat the symptoms of the disease. A major goal of Parkinson's disease research is the development of disease-modifying drugs that slow or stop the neurodegenerative process. Drugs that enhance the intracerebral dopamine concentrations or stimulate dopamine receptors remain the mainstay treatment for motor symptoms. Immunomodulatory therapeutic strategies aiming to attenuate PD neurodegeneration have become an attractive option and warrant further investigation.

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Authors+Show Affiliations

De Virgilio A
Department Organs of Sense, ENT Section, 'Sapienza' University of Rome, Viale del Policlinico 155, 00100, Rome, Italy; Department of Surgical Science, 'Sapienza' University of Rome, Viale del Policlinico 155, 00100, Rome, Italy.
Greco A
Department Organs of Sense, ENT Section, 'Sapienza' University of Rome, Viale del Policlinico 155, 00100, Rome, Italy.
Fabbrini G
Department of Neurology and Psychiatry, 'Sapienza' University of Rome, Viale del Policlinico 155, 00100, Rome, Italy.
Inghilleri M
Department of Neurology and Psychiatry, 'Sapienza' University of Rome, Viale del Policlinico 155, 00100, Rome, Italy.
Rizzo MI
Department Organs of Sense, ENT Section, 'Sapienza' University of Rome, Viale del Policlinico 155, 00100, Rome, Italy; Department of Surgical Science, 'Sapienza' University of Rome, Viale del Policlinico 155, 00100, Rome, Italy. Electronic address: mariaidarizzo@gmail.com.
Gallo A
Department of Medico-Surgical Sciences and Biotechnologies, Otorhinolaryngology Section, 'Sapienza' University of Rome, Corso della Repubblica, 79, 04100 Latina, Italy.
Conte M
Department Organs of Sense, ENT Section, 'Sapienza' University of Rome, Viale del Policlinico 155, 00100, Rome, Italy.
Rosato C
Department of Medico-Surgical Sciences and Biotechnologies, Otorhinolaryngology Section, 'Sapienza' University of Rome, Corso della Repubblica, 79, 04100 Latina, Italy.
Ciniglio Appiani M
Department Organs of Sense, ENT Section, 'Sapienza' University of Rome, Viale del Policlinico 155, 00100, Rome, Italy; Department of Surgical Science, 'Sapienza' University of Rome, Viale del Policlinico 155, 00100, Rome, Italy.
de Vincentiis M
Department Organs of Sense, ENT Section, 'Sapienza' University of Rome, Viale del Policlinico 155, 00100, Rome, Italy.

MeSH

AnimalsAutoimmunityBrainDisease ProgressionHumansInflammationNeuronsParkinson Disease

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

27497913

Citation

De Virgilio, Armando, et al. "Parkinson's Disease: Autoimmunity and Neuroinflammation." Autoimmunity Reviews, vol. 15, no. 10, 2016, pp. 1005-11.
De Virgilio A, Greco A, Fabbrini G, et al. Parkinson's disease: Autoimmunity and neuroinflammation. Autoimmun Rev. 2016;15(10):1005-11.
De Virgilio, A., Greco, A., Fabbrini, G., Inghilleri, M., Rizzo, M. I., Gallo, A., Conte, M., Rosato, C., Ciniglio Appiani, M., & de Vincentiis, M. (2016). Parkinson's disease: Autoimmunity and neuroinflammation. Autoimmunity Reviews, 15(10), 1005-11. https://doi.org/10.1016/j.autrev.2016.07.022
De Virgilio A, et al. Parkinson's Disease: Autoimmunity and Neuroinflammation. Autoimmun Rev. 2016;15(10):1005-11. PubMed PMID: 27497913.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Parkinson's disease: Autoimmunity and neuroinflammation. AU - De Virgilio,Armando, AU - Greco,Antonio, AU - Fabbrini,Giovanni, AU - Inghilleri,Maurizio, AU - Rizzo,Maria Ida, AU - Gallo,Andrea, AU - Conte,Michela, AU - Rosato,Chiara, AU - Ciniglio Appiani,Mario, AU - de Vincentiis,Marco, Y1 - 2016/08/04/ PY - 2016/8/8/entrez PY - 2016/8/9/pubmed PY - 2017/1/4/medline KW - Autoimmunity KW - Inflammation KW - Lewy bodies KW - Neurodegenerative disease KW - Olfactory dysfunction KW - Parkinson KW - α-Synuclein SP - 1005 EP - 11 JF - Autoimmunity reviews JO - Autoimmun Rev VL - 15 IS - 10 N2 - Parkinson's disease is a neurodegenerative disease that causes the death of dopaminergic neurons in the substantia nigra. The resulting dopamine deficiency in the basal ganglia leads to a movement disorder that is characterized by classical parkinsonian motor symptoms. Parkinson's disease is recognized as the most common neurodegenerative disorder after Alzheimer's disease. PD ethiopathogenesis remains to be elucidated and has been connected to genetic, environmental and immunologic conditions. The past decade has provided evidence for a significant role of the immune system in PD pathogenesis, either through inflammation or an autoimmune response. Several autoantibodies directed at antigens associated with PD pathogenesis have been identified in PD patients. This immune activation may be the cause of, rather than a response to, the observed neuronal loss. Parkinsonian motor symptoms include bradykinesia, muscular rigidity and resting tremor. The non-motor features include olfactory dysfunction, cognitive impairment, psychiatric symptoms and autonomic dysfunction. Microscopically, the specific degeneration of dopaminergic neurons in the substantia nigra and the presence of Lewy bodies, which are brain deposits containing a substantial amount of α-synuclein, have been recognized. The progression of Parkinson's disease is characterized by a worsening of motor features; however, as the disease progresses, there is an emergence of complications related to long-term symptomatic treatment. The available therapies for Parkinson's disease only treat the symptoms of the disease. A major goal of Parkinson's disease research is the development of disease-modifying drugs that slow or stop the neurodegenerative process. Drugs that enhance the intracerebral dopamine concentrations or stimulate dopamine receptors remain the mainstay treatment for motor symptoms. Immunomodulatory therapeutic strategies aiming to attenuate PD neurodegeneration have become an attractive option and warrant further investigation. SN - 1873-0183 UR - https://www.unboundmedicine.com/medline/citation/27497913/Parkinson's_disease:_Autoimmunity_and_neuroinflammation_ DB - PRIME DP - Unbound Medicine ER -