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Lipopolysaccharide-Induced Neuroinflammation as a Bridge to Understand Neurodegeneration

期刊

出版社

MDPI
DOI: 10.3390/ijms20092293

关键词

lipopolysaccharide; inflammation; neurodegeneration; Alzheimer's disease; Parkinson's disease; amyotrophic lateral sclerosis; Huntington's disease

资金

  1. Fundacao de Amparo a Pesquisa do Estado de Minas Gerais (FAPEMIG) [APQ-02044-15]
  2. Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq) [424588/2016-1]
  3. Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES)
  4. CNPq [310347/2018-1]
  5. University of Freiburg Library

向作者/读者索取更多资源

A large body of experimental evidence suggests that neuroinflammation is a key pathological event triggering and perpetuating the neurodegenerative process associated with many neurological diseases. Therefore, different stimuli, such as lipopolysaccharide (LPS), are used to model neuroinflammation associated with neurodegeneration. By acting at its receptors, LPS activates various intracellular molecules, which alter the expression of a plethora of inflammatory mediators. These factors, in turn, initiate or contribute to the development of neurodegenerative processes. Therefore, LPS is an important tool for the study of neuroinflammation associated with neurodegenerative diseases. However, the serotype, route of administration, and number of injections of this toxin induce varied pathological responses. Thus, here, we review the use of LPS in various models of neurodegeneration as well as discuss the neuroinflammatory mechanisms induced by this toxin that could underpin the pathological events linked to the neurodegenerative process.

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