Neuroinflammation is involved in neurodegenerative disorders such as amyotrophic lateral sclerosis, Huntington's disease, multiple sclerosis, Parkinson's disease, and Alzheimer disease (AD). AD, the most common form of dementia in the elderly, is characterized by specific pathologies in the brain. Currently, it is thought that longitudinal pathophysiological processes cause AD patients' brains to be in a state of chronic neuroinflammation; additionally, reactive glial cells, the innate immune system in the brain, contribute to AD pathogenesis. However, the detailed molecular and cellular mechanisms underlying this pathogenesis are still unclear because of the disease complexities. In addition, because the existing animal models of AD are not accurate and reproducible, the development of therapeutic strategies for the disease is slow. To overcome these obstacles, we have to revalidate the previously obtained results whether they are beneficial or detrimental, and promote the elucidation of the pathogenic mechanisms of AD using relevant animal models. This review reconsiders insights of the current situation of AD research and shares perspectives for understanding AD pathogenesis when considered as a whole body disorder.
CITATION STYLE
Saito, T. (2016). Chronic Neuroinflammation Underlying Pathogenesis of Alzheimer’s Disease. In Chronic Inflammation (pp. 661–671). Springer Japan. https://doi.org/10.1007/978-4-431-56068-5_50
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