Modulation of inflammation in transgenic models of Alzheimer's disease

• Published in: Journal of neuroinflammation Vol. 11; no. 1; p. 25
• Main Authors: Birch, Amy M, Katsouri, Loukia, Sastre, Magdalena
• Format: Journal Article
• Language: English
• Published: England BioMed Central Ltd 03.02.2014; BioMed Central
• Subjects: Advertising executives; Alzheimer Disease - complications; Alzheimer Disease - genetics; Alzheimer's disease; Amyloid beta-protein; Animals; Animals, Genetically Modified; Disease Models, Animal; Encephalitis - etiology; Encephalitis - genetics; Health aspects; Humans; Inflammation; Mutation; Nitric oxide; Physiological aspects; Review; Rodents
• ISSN: 1742-2094; 1742-2094
• DOI: 10.1186/1742-2094-11-25

Over the past decade the process of inflammation has been a focus of increasing interest in the Alzheimer's disease (AD) field, not only for its potential role in neuronal degeneration but also as a promising therapeutic target. However, recent research in this field has provided divergent outcomes, largely due to the use of different models and different stages of the disease when the investigations have been carried out. It is now accepted that microglia, and possibly astrocytes, change their activation phenotype during ageing and the stage of the disease, and therefore these are important factors to have in mind to define the function of different inflammatory components as well as potential therapies. Modulating inflammation using animal models of AD has offered the possibility to investigate inflammatory components individually and manipulate inflammatory genes in amyloid precursor protein and tau transgenics independently. This has also offered some hints on the mechanisms by which these factors may affect AD pathology. In this review we examine the different transgenic approaches and treatments that have been reported to modulate inflammation using animal models of AD. These studies have provided evidence that enhancing inflammation is linked with increases in amyloid-beta (Aβ) generation, Aβ aggregation and tau phosphorylation. However, the alterations on tau phosphorylation can be independent of changes in Aβ levels by these inflammatory mediators.