Pathologic hallmarks of Alzheimer's disease (AD) include neuritic plaques, neurofibrillary tangles and degeneration of neurons in the hippocampus and cortex of the brain. A study in Scientific Reports reports that increasing a protein called neuregulin-1 (NRG1) in the brain significantly reduces symptoms of Alzheimer's disease (AD) in experimental mice. NRG1 performs multiple functions in the brain, and it can exist in different forms. Some studies have indicated that it may be a therapeutic target for schizophrenia, Parkinson's disease and some other brain diseases. In this study, the Salk Institute researchers worked to test if this protein influences cognitive function and neuropathology in AD. One of two forms of NRG1 was overexpressed in the hippocampus of a AD mouse model. The hippocampus is a brain region vital to memory and learning. The researchers then performed Morris water-maze test to study the ability of spatial memory in these mice, and found that both forms of NRG1 elevated their performance. In addition, the levels of some cellular markers of AD, such as Aβ peptides and plaques, were significantly reduced. Further experiments showed that NRG1 greatly increased expression of Aβ-degrading enzyme neprilysin (NEP). This might be one way that NRG1 uses to produce beneficial effects. The researchers are now studying other possible mechanisms. Since NRG1 has been found to be able to cross the blood brain barrier, the study raises the possibility of using the protein as a drug. Remarkably, there is evidence that excessive NRG1 harms brain function. According to the lead researcher of the new study, Prof. Kuo-Fen Lee, this protein helps explore the link between AD and other brain diseases. In this research, the investigators used various antibodies, such as rabbit polyclonal antibody against NRG1, monoclonal antibody against NEP, and recombinant proteins, such as recombinant soluble human type I NRG1 and Recombinant human type III NRG1 (Other recombinant protein of CusAb: Recombinant ITGB1)
