Inflammation and Parkinson's Disease
1Clinical and Experimental Neuroscience, CIBERNED, Department of Anatomy, School of Medicine, University of Murcia, Campus de Espinardo, 30100 Murcia, Spain
2CRICM, INSERM/UPMC UMR_S975 (ex U679), CNRS UMR 7225, Experimental Therapeutics on Neurodegeneration, Hôpital de la Salpêtrière, 47 Boulevard de l'Hôpital, 75013 Paris, France
3Department of Pharmacology, University of New South Wales, Wallace Wurth Building, Sydney, NSW 2052, Australia
4Instituto Leloir, IIBBA-CONICET, Avenue Patricias Argentinas 435 (1405), Buenos Aires, Argentina
Inflammation and Parkinson's Disease
Description
In the field of neurodegenerative diseases, the concept of noncell autonomous disease mechanisms suggests that neurodegeneration is not just mediated by damages within the affected neurons but is also influenced by interactions with neighboring glial and peripheral immune cells invading the injured brain. The neuroinflammatory response, a major component of these noncell autonomous mechanisms, produces culprits that could represent the core of the progressive nature of neurodegenerative diseases including Parkinson's disease (PD). Indeed, growing evidence from epidemiological, post mortem, and animal studies suggest that both the innate and adaptive arms of the immune system could participate in the progression of dopaminergic cell death in PD. Yet, in spite of unquestionable major advances made in the field of neuroimmune interactions in PD, the precise identity, origin, and function of the various innate and adaptive immune cells involved in response to dopaminergic degeneration have not been completely identified. Settling these questions is crucial to accurately depict the mechanism of cell death in PD and also to develop therapeutic strategies that selectively target the cytotoxic arm without altering the beneficial function of immune cells.
The main focus of this special issue will be on clinical and basic studies investigating all aspects of the inflammatory response and neuron-immune interactions in PD. We particularly take interest in manuscripts reporting new clinical evidences showing inflammatory alterations in patients with PD, new antiinflammatory treatments that may improve their prognosis, as well as studies of basic science in disease models depicting the mechanisms of neuroinflammation and/or demonstrating the beneficial effects of antiinflammatory drugs. Main topics include, but are not limited to:
- Systemic immune alterations/deviations in PD patients: cellular and molecular characteristics of peripheral innate and adaptive immune responses
- Central immune responses in PD: glial cell response to dopaminergic degeneration, involvement of peripheral immune cells in the central inflammatory response
- Immunity and PD etiopathogenesis: impact of systemic inflammation, viral infection, and environmental factors on risk or disease progression
- Preclinical studies of immune-based therapeutics: antiinflammatory drugs and immunization
- Clinical studies: case reports and clinical trials
- Epidemiological studies: large population studies correlating the influence of antiinflammatory treatments, genetic polymorphisms on inflammatory genes or infections, and risk or PD progression
Both original scientific papers and review articles on the above topics will be considered for publication.
Before submission authors should carefully read over the journal's Author Guidelines, which are located at http://www.hindawi.com/journals/pd/guidelines/. Prospective authors should submit an electronic copy of their complete manuscript through the journal Manuscript Tracking System at http://mts.hindawi.com/ according to the following timetable: