Parkinson's Disease and Systemic Inflammation

被引:157
|
作者
Ferrari, Carina C. [1 ]
Tarelli, Rodolfo [1 ]
机构
[1] Fdn Inst Leloir, Lab Terapias Regenerativas & Protectoras Sistema, Buenos Aires, DF, Argentina
关键词
BLOOD-BRAIN-BARRIER; CENTRAL-NERVOUS-SYSTEM; NONSTEROIDAL ANTIINFLAMMATORY DRUGS; NITRIC-OXIDE SYNTHASE; GROWTH-FACTOR-ALPHA; REGULATORY T-CELLS; SICKNESS BEHAVIOR; ACUTE-PHASE; AGED MICE; RAT MODEL;
D O I
10.4061/2011/436813
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Peripheral inflammation triggers exacerbation in the central brain's ongoing damage in several neurodegenerative diseases. Systemic inflammatory stimulus induce a general response known as sickness behaviour, indicating that a peripheral stimulus can induce the synthesis of cytokines in the brain. In Parkinson's disease (PD), inflammation was mainly associated with microglia activation that can underlie the neurodegeneration of neurons in the substantia nigra (SN). Peripheral inflammation can transform the "primed" microglia into an "active" state, which can trigger stronger responses dealing with neurodegenerative processes. Numerous evidences show that systemic inflammatory processes exacerbate ongoing neurodegeneration in PD patient and animal models. Anti-inflammatory treatment in PD patients exerts a neuroprotective effect. In the present paper, we analyse the effect of peripheral infections in the etiology and progression in PD patients and animal models, suggesting that these peripheral immune challenges can exacerbate the symptoms in the disease.
引用
收藏
页数:9
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