Topic: NF-κB

Microglia are the resident CNS macrophages of the brain parenchyma. They have many and opposing roles in health and disease, ranging from inflammatory to anti-inflammatory and protective functions, depending on the developmental stage and the disease context. In Multiple Sclerosis, microglia are involved to important hallmarks of the disease, such as inflammation, demyelination, axonal damage and remyelination, however the exact mechanisms controlling their transformation towards a protective or devastating phenotype during the disease progression remains largely unknown until now. We wish to

Spinal Muscular Atrophy (SMA) is a genetic disorder resulting from the deletion or mutation of the SMN1 gene (Survival Motor Neuron 1). The reduction in SMN protein levels leads to the degeneration of motor neurons in the spinal cord, giving rise to typical clinical manifestations of the disease, such as muscular weakness and atrophy. At the cellular level, SMN is part of a macromolecular machinery referred to the SMN complex, comprising various proteins, including Gemin3. Among other functions, Gemin3 regulates the intracellular survival signaling pathway NF-κB. In the context of SMA disease,

Acupuncture is a component of the complex therapeutic and healthcare system of China that has been used for more than 2500 years. Oriental medicine describes how acupoints are associated with internal organs and acupuncture treatment on back-shu points (BSPs) has received attention owing to its ability to control the function of visceral organs. Previous studies suggested that an acupoint is one form of neurogenic inflammation on the skin. In this study, we compared of the anatomic location between neurogenic inflammatory areas in the skin (neurogenic spots) and traditional acupuncture points

Patients with liver cirrhosis show hyperammonemia and peripheral inflammation and may show hepatic encephalopathy with cognitive impairment, reproduced by rats with chronic hyperammonemia. Peripheral inflammation induces neuroinflammation in hippocampus of hyperammonemic rats, altering neurotransmission and leading to cognitive impairment. Extracellular vesicles (EVs) may transmit pathological effects from the periphery to the brain. The aims were to assess whether EVs from plasma of hyperammonemic rats (HA-EVs) induce cognitive impairment and to identify the underlying mechanisms.HA-EVs were