There is a significant association between the pathogenesis of Alzheimer's disease (AD) and type 2 diabetes mellitus (T2DM), in which the blood-brain barrier (BBB), as an essential bridge connecting the periphery to the central nervous system, maybe a vital link in revealing the mechanism of the association between the two diseases. The function of the T2DM blood-brain barrier and its influence on the pathogenesis of AD remains unclear. We found reduced Glut-1 and Claudin-5 immunopositive reactive regions in the brains of spontaneous T2DM cynomolgus monkeys by multiple immunological experiments, suggesting dysfunctional transport and impaired integrity of the blood-brain barrier. Meanwhile, different degrees of AD-like pathology formation were found in the brains of spontaneous T2DM cynomolgus monkeys and were positively correlated with the degree of blood-brain barrier damage. The present study demonstrates that T2DM leads to impairmed of blood-brain barrier integrity, subsequently affecting AD pathogenesis.
Neuroinflammation induced by activated microglia is a typical pathological feature in most neurodegenerative diseases. Generally, inhibition of neuroinflammation could attenuate damage of brain in neurodegenerative diseases. Photobiomodulation (PBM) has been proved to suppress neuroinflammation by decreasing microglial activation. However, the underlying mechanisms of PBM on microglial inflammation remain unclear. Herein, we studied the effects of mitochondrial function on PBM regulated microglial inflammation. The results showed that PBM attenuates lipopolysaccharide (LPS)-induced microglial proinflammatory response while ameliorating mitochondrial dysfunction. Further study revealed that PBM promotes mitophagy in microglia exposed to LPS. In addition, we found that 3- methyladenine (3-MA), the autophagy inhibitor, disrupts microglial mitophagy and reverses the protective effect of PBM on inflammation. Taken together, these studies underline the significance of mitophagy in suppressing inflammation and enhancing mitochondrial function in activated microglia under PBM treatment. Our research may supply a potential strategy to control the progression of neuroinflammation.
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