Neuroinflammation in Alzheimer's, Parkinson's and Huntington's Diseases
(2014) Neuroinflammation and CNS Disorders — ISBN: [9781118406410], p. 111-150, published
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- Abstract
- Neuroinflammation and oxidative stress are involved in the pathogenesis of Alzheimer's, Parkinson's and Huntington's diseases. This is caused mainly by the presence of misfolded proteins which act as a catalyst for the activation and sustained activity of glial cells. Activated microglial cells are involved in both the initiation and progression of the disease, which will lead to the release of many pro-inflammatory mediators which induce neuronal injury and death. In addition, astrocytes may play an important role; their ability to secrete important neurotrophic factors may be impaired, while the release of pro-inflammatory cytokines may contribute to the cellular destruction. Activation of the innate and adaptive immune responses is evident in these diseases, while the production of reactive oxygen and nitrogen species will contribute to the neuronal destruction
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Citations
Sastre, M., Katsouri, L., Birch, A. M., Renziehausen, A., Dexter, D. T., Crichton, R., & Ward, R. (2014). Neuroinflammation in Alzheimer’s, Parkinson’s and Huntington’s Diseases. In Nicola Woodroofe, Sandra Amor (ed.), Neuroinflammation and CNS Disorders (p. p. 111-150). Wiley-Blackwell Publishing Ltd. https://doi.org/10.1002/9781118406557.ch6