Issue Cover (April 2019)

Front cover:Reductions in the sensitivity of the brain insulin receptor (IR) have been linked to the appearance of cognitive dysfunctions. This relationship has been demonstrated both by preclinical and clinical data and has been labelled as Type 3 Diabetes. It is believed to be the previous step to the appearance of sporadic or late ‐onset Alzheimer’s disease. The c‐Jun N‐terminal Kinases (JNK) are one of the many regulator of the IR. In order to investigate this mechanism, Mapk9 gene knock‐out transgenic mice (JNK2 knock‐out) together with a palmitic acid‐enriched diet (high‐fat diet; HFD) were used. We found t hat the lack of JNK2 and the HFD diet reduced the sensitivity of the IR and increased body weight. Also, proteins like the Protein Tyrosine Phosphatase 1B (PTP1B) and Suppressor of Cytokine Signalling 3 (SOCS3), which have been described to regulate negatively the IR, showed up‐regulation. Further more, an impairment on cognition was demonstrated but, interestingly, the JNK2 knock‐out transgenic mice showed no neuroinflammatory reactivity. The data of the present study points out to the relevance of JNK2 in the cells and supports the relationship between metabolic alterations and cognitive impairment.Image content: Microscope image from an immunofluorescence assay for the detection of the Glial Fibrillary Acidic Protein (GFAP; red), a biomarker of astrocytes. This image captures de dentate gyrus of the hippocampus of a mice fed with HFD and shows ...
Source: Journal of Neurochemistry - Category: Neuroscience Tags: Issue Cover Source Type: research