Peer-Reviewed Journal Details
Mandatory Fields
Walsh, S,Gavin, A,Wyatt, S,O'Connor, C,Keeshan, K,Nolan, YM,O'Keeffe, GW,Sullivan, AM
2015
January
The International journal of neuroscience
Knockdown of interleukin-1 receptor 1 is not neuroprotective in the 6-hydroxydopamine striatal lesion rat model of Parkinson's disease
Validated
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Optional Fields
neuroinflammation shRNA dopaminergic neuron degeneration NECROSIS-FACTOR-ALPHA NEURODEGENERATIVE DISEASES DOPAMINERGIC-NEURONS CORRIDOR TASK ANIMAL-MODEL GLIAL-CELLS BRAIN NEUROINFLAMMATION SUSCEPTIBILITY ACTIVATION
125
70
77
It is well established that neuroinflammation is associated with the progression of many neurodegenerative diseases, including Parkinson's disease (PD). Activated microglia and elevated levels of pro-inflammatory cytokines such as interleukin-1 beta (IL-1 beta) have been found in the brain and cerebrospinal fluid of PD patients, suggesting that IL-1 beta may be involved in the pathogenesis of this disease. This study aimed to knock down the expression of the interleukin-1 type 1 receptor (IL-1R1) to evaluate any potential therapeutic effect of limiting the action of IL-1 beta in the substantia nigra following a unilateral intrastriatal 6-hydroxydopamine (6-OHDA) lesion in rats. Adult Sprague-Dawley rats received intranigral injections of shRNA specific for IL-1R1, followed 2 weeks later by intrastriatal 6-OHDA. Injection of IL-1R1 shRNA did not prevent 6-OHDA-induced loss of motor function or loss of nigral dopamine neurons. IL-1R1 expression was increased in the midbrain following 6-OHDA injection; this effect was attenuated in 6-OHDA-treated animals that had received IL-1R1 shRNA. These data suggest that while IL-1R1 was increased in 6-OHDA-treated animals and reduced following shRNA injection, the neurodegeneration induced by 6-OHDA was not mediated through IL-1R1.
10.3109/00207454.2014.904304
Grant Details