English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Glial activation and increased inflammation characterize neuropathology in Alzheimer's disease (AD). The aim was to develop a model for studying phagocytosis of beta-amyloid (Abeta) peptide by human microglia and to test effects thereupon by immunomodulatory substances. Human CHME3 microglia showed intracellular Abeta(1-42) colocalized with lysosome-associated membrane protein-2, indicating phagocytosis. This was increased by interferon-gamma, and to a lesser degree with Protollin, a proteosome-based adjuvant. Secretion of brain-derived neurotrophic factor (BDNF) was decreased by Abeta(1-42) and by interferon-gamma and interleukin-1beta. These cytokines, but not Abeta(1-42), stimulated interleukin-6 release. Microglia which phagocytosed Abeta(1-42) exhibited a higher degree of expression of interleukin-1 receptor type I and inducible nitric oxide synthase. In conclusion, we show that human microglia are able to phagocytose Abeta(1-42) and that this is associated with expression of inflammatory markers. Abeta(1-42) and interferon-gamma decreased BDNF secretion suggesting a new neuropathological role for Abeta(1-42) and the inflammation accompanying AD.

Effects of Immunomodulatory Substances on Phagocytosis of A by Human Microglia