Issue Cover (February 2016)

Front cover : Epidemiological and experimental studies indicate individuals with Alzheimer's disease (AD) have impaired glucose regulation and increased incidence of Type 2 diabetes (T2D). However, a comprehensive understanding of the underlying mechanisms of the effects of AD genotype on T2D pathology is still lacking. A recent concept, that AD is a multifactorial systemic disease, suggests the potential involvement of the peripheral tissue as a link between T2D and AD. The image shows representative images of H&E staining of liver sections of 14‐week‐old female APPSWE/PSEN1dE9 (AD) mice are subjected to high‐fat diet (HFD, 45% kcal fat content) for 22 weeks. The data reveal that HFD‐fed AD mice had much less hepatic lipid droplets than their wild type controls. The study reveals that early‐stage inflammation in the liver of AD mice blunts hepatic SREBP–1–mediated de novo lipogenesis, leading to the resistance of AD mice to HFD‐induced fatty liver. However, AD mice exhibit higher fasting glucose and greater impaired glucose tolerance, implying inactivation of hepatic lipogenesis drives substrate flux to glucose production for hyperglycemia and insulin resistance in T2D progression.Read the full article ‘ Early inflammation‐associated factors blunt sterol regulatory element‐binding proteins–1–mediated lipogenesis in high‐fat diet‐fed APP SWE /PSEN1dE9 mouse model of Alzheimer's disease ’ by Y. Tang, Y. Peng, J. Liu, L. Shi, Y. Wang, J. Long and J. Liu ( J. Neurochem . 2016, vol. 136 (4), pp. 791–803) on doi: 10.1111/jnc.13437