Microglia activation is the major component of inflammation that constitutes the characteristic of neurodegenerative disease. A large amount of researches have demonstrated that inflammation involved in the pathogenesis of PD process activated microglia acting on the neurons through the release of a variety of inflammatory factors. However, the molecular mechanism underlying how it does work on neurons is still unclear. Here, we show that intracerebral injections of LPS induced Parkinson’s disease pathology in C57BL/6J mice. Furthermore, study on the dynamic changes in Synaptic vesicle-associated protein and axonal transport Protein in this process. The results indicated that after administration of LPS in the brain, the inflammatory levels of TNF-α and IL-1β both are elevated, and have a time-dependent. 1. Introduction Parkinson’s disease (PD) is primarily an age-related debilitating neurodegenerative disorder characterized by a selective and gradual loss of dopaminergic (DA) innervations from the substantia nigra pars compacta (SNpc) to the striatum (caudate and putamen) of the basal ganglia [1, 2]. Progressive degeneration of the nigrostriatal DA pathway eventually leads to the development of clinical symptoms that include bradykinesia, rigidity, tremor, and defective gait, mostly in people over the age of 60 [3]. Postmortem confirmative diagnosis often detects a massive loss of SNpc DA neurons and the presence of the characteristic cytoplasmic inclusions called Lewy bodies in survived neurons. Except for a small fraction of early onset cases of PD that are linked to mutations in a dozen genes, most cases of PD are idiopathic [1, 4]. Risk factors for idiopathic PD include age, genetic predisposition, and exposure to agents such as pesticides, metals, and infectious agents [5]. Findings from epidemiological studies and analysis of postmortem PD brains and animal PD models have provided increasing evidence to support a role for inflammation in the brain in the pathogenesis of PD [6]. And in the process of Parkinson’s disease (PD), neuroinflammation appears early and nearly persists throughout the disease course [7]. Moreover, during the early life occurrence of inflammation in the brain, as a consequence of either brain injury or exposure to infectious agents, This process may play a role in the pathogenesis of PD [8]. Microglia are the resident immune cells in the brain and have critical roles in immune surveillance under normal conditions. However, activated microglia release pro-inflammatory molecules such as IL-1β, tumor necrosis factorα (TNF-α),
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