MiR-18a-LncRNA NONRATG-022419 pairs targeted PRG-1 regulates diabetic induced cognitive impairment by regulating NGF\BDNF-Trkb signaling pathway.

Background: Diabetic encephalopathy (DE) is considered as one of the complications of diabetes,which is associated with cognitive impairment in the pathological process of development. Up to now, phospholipid phosphatase related 4 (Plppr4), also known as plasticity related gene 1 (PRG-1) has been revealed its important role in neuroplasticity. However, the underlying mechanisms of Plppr4 on the basis of diabetic-induced cognitive dysfunction (DCD) are still unknown.

The integrated analysis and underlying mechanisms of FNDC5 on diabetic induced cognitive deficits.

Objectives: Chronic hyperglycemia is considered as an important factor to promote the neurodegenerative process of brain, and the synaptic plasticity as well as heterogeneity of hippocampal cells are thought to be associated with cognitive dysfunction in the early process of neurodegeneration. To date, fibronectin type III domain-containing protein 5 (FNDC5) has been highlighted its protective role in multiple neurodegenerative diseases. However, the potential molecular and cellular mechanisms of FNDC5 on synaptic plasticity regulation in cognitive impairment (CI) induced by diabetics are still need to known.

The Molecular Mechanism of CoenzymeQ10 on Pyroptosis and its Related Diseases: A Review.

In recent years, cell pyroptosis has made it widely concerned. Pyroptosis is characterized by the activation of pathways leading to the activation of NLRP3 inflammasome and its downstream effector, such as interleukin (IL)-1β and IL-18, which has close relationship with inflammation. Recent evidence supports that CoenzymeQ10 (CoQ10) reduces related inflammatory factors (NLRP3, IL-1β and IL-18), which are associated with cell pyroptosis.