Skip to main content
. Author manuscript; available in PMC: 2018 May 1.
Published in final edited form as: Biochim Biophys Acta. 2016 May 6;1863(5):1037–1045. doi: 10.1016/j.bbadis.2016.04.017

Figure 4. Neuroinflammation in the Diabetic brain.

Figure 4

Brain inflammation in diabetes is considered to result from peripheral inflammation. Cytokines produced by macrophages can pass through the blood brain barrier (BBB). However the less understood area is the potential direct effects of saturated fatty acids (SFA) and advanced glycation end products (AGEs) on neurons astrocytes and microglia, the resident macrophages of the brain. Increased uptake of fatty acids by the brain in metabolic syndrome has been reported. Neurotoxins generated by astroglia cause injuries to neurons. Stress signals released by dying neurons can further activate the glial cells, thus leading to a vicious cycle. Activators of SIRT1 have two beneficial therapeutic actions, namely, increasing neuronal mitochondrial biogenesis and anti-inflammatory action in glial cells.