Lipopolysaccharide Animal Models for Parkinson's Disease
Figure 1
LPS induces progressive neurotoxicity. In response to LPS stimuli, microglial cells are readily activated. It is demonstrated that LPS binds to specific receptors, for example, CD14/TLR4/LBP receptor complex on the microglia, to induce microglial activation. Uncontrolled microglial activation produce a variety of neurotoxic factors such as proinflammatory cytokines (IL-1, TNF-α, IL-6), NO, PGE2, and , which lead to neuronal damage or death through a cascade of events such as oxidative/nitrative stress, mitochondrial dysfunction, and apoptosis. Moreover, damaged neurons may emit injury signals to cause microglia activation, which is defined as reactive microgliosis. The injury signals could be neuromelanin and α-synuclein released by injured dopaminergic neurons. This microglial-neuronal interaction will be reinforced and become a self-amplifying cycle of neuronal injury and microglial activation, which may finally result in the neurodegenerative disease.
