Studies reveal the mechanism by which Alzheimer's occurs

Alzheimer's disease is a neurodegenerative disease characterized by the accumulation of β amyloid protein lumps in the brain. Revealing the causes of these plaques, known as plaques, and their role in disease progression is currently a hot topic of research in this area and is critical to the development of prevention and treatment strategies.Recent studies have found β-amyloid proteins with antiviral and antibacterial properties, suggesting a possible link between an immune response to infection and the development of Alzheimer's disease.Chemical biologists at the Sloan Kettering Institute have now found clear evidence of this link: a protein called IFITM3 is involved in the immune response to pathogens and plays a key role in the accumulation of β amyloid proteins in plaques."We know that the immune system works in Alzheimer's disease, for example, by helping to remove β-amyloid plaques from the brain," said study author Yueming Li, a chemical biologist at SKI. But this is the first direct evidence that the immune β promotes the production of this protein- amyloid plaque. Inpaper published September 2 in the journal nature, the authors and others show that IFITM3 alters the enzyme activity of the γ-secretase, which is usually responsible for cutting pregenital proteins into β-amyloid fragments.They found that removing IFITM3 reduced γ activity of the enzyme, thereby reducing the number of amyloid plaques formed in mouse models of the disease.Inflammation of nerves or the brain has become an important topic in the study of Alzheimer's disease. Inflammatory markers, such as some called cytokines, are highly expressed in mouse models of Alzheimer's disease and in the brains of patients with Alzheimer's disease. For the first time, the study established a direct link between inflammation and plaque development through IFETM3.IFITM3 begins by invading viruses and bacteria in response to the activation of the immune system. Because new research suggests that IFITM3 directly contributes to plaque formation, it means that viral and bacterial infections may increase the risk of developing Alzheimer's disease. In fact, the authors and others found that IFITM3 levels in human brain samples were associated with levels of certain viral infections, γ-secretion enzyme activity, and the production of β-amyloid proteins.The researchers found that age was the number one risk factor for Alzheimer's disease, with levels of inflammatory markers and IFITM3 increasing with age. They also found that IFITM3 levels were relatively high in patients with advanced Alzheimer's disease, meaning that IFITM3 could be used as a biomarker to identify some patients who might benefit from treatments for IFITM3.The researchers' next project is to study how IFIDM3 interacts with γ-secretases at the molecular and atomic levels and how it is involved in neuroinstatics in animal models. They will also explore IFITM3 as a biomarker of the disease and as a potential target for new drugs designed to treat the disease. (Bio Valley Bioon.com)