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Modulation of inflammation in transgenic models of Alzheimer's disease

Birch, AM; Katsouri, L; Sastre, M; (2014) Modulation of inflammation in transgenic models of Alzheimer's disease. Journal of Neuroinflammation , 11 , Article 25. 10.1186/1742-2094-11-25. Green open access

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Abstract

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.

Type: Article
Title: Modulation of inflammation in transgenic models of Alzheimer's disease
Open access status: An open access version is available from UCL Discovery
DOI: 10.1186/1742-2094-11-25
Publisher version: https://doi.org/10.1186/1742-2094-11-25
Language: English
Additional information: This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
Keywords: Science & Technology, Life Sciences & Biomedicine, Immunology, Neurosciences, Neurosciences & Neurology, Inflammation, Microglia, Astrocytes, Amyloid, Tau, Transgenics, Anti-inflammatory, AMYLOID PRECURSOR PROTEIN, NONSTEROIDAL ANTIINFLAMMATORY DRUGS, CENTRAL-NERVOUS-SYSTEM, EXACERBATES TAU PATHOLOGY, GAMMA-SECRETASE MODULATOR, NECROSIS-FACTOR-ALPHA, MOUSE MODEL, MICROGLIAL ACTIVATION, A-BETA, PLAQUE DEPOSITION
UCL classification: UCL
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Life Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Life Sciences > The Sainsbury Wellcome Centre
URI: https://discovery.ucl.ac.uk/id/eprint/10035010
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