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Combined with A beta, microglia can be activated and produce toxic products such as free radical, cytokine, and glutamate agonists, which will accelerate neuronal death [ 10].
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Here we reveal a new application of ptychography for long-term imaging of complex primary neuronal cultures10, where phenotypic behaviour of microglia can be studied.
Butovsky O, Bukshpan S, Kunis G, Jung S, Schwartz M. Microglia can be induced by IFN-gamma or IL-4 to express neural or dendritic-like markers.
That means activated microglia can be either friends or foes to neighbouring neurons.
Thus, it seems that microglia can be a double-edged sword [53].
Activated brain microglia can be neuroprotective by assuming an M2-like phenotype [56 58], a phenomena similar to what occur in macrophages.
The local density of microglia can be as great as 20 times higher in glioma than normal brain tissue (Hussain et al., 2006b).
In addition, secretion of Aβ oligomer from Aβ-phagocytized microglia was also enhanced by CCL2 (Fig. 7B), demonstrating that microglia can be a source of Aβ oligomer formation.
In the diseased brain microglia can be stimulated by a variety of sterile and pathogenic stimuli.
Cell division by microglia can be considered an ongoing feature of microglia in pathology-rich areas, and is required to replace these short-lived cells.
In Alzheimer disease microglia can be beneficial by phagocytosing Aβ or harmful by secretion of neurotoxins.
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