The β-Hairpins peptides affect Alzheimer’s Disease by Regulating theInflammation of Astroglial and Microglial Cell

Abstract

Alzheimer’s disease is the most common type of brain disease now present in the world. Patients with Alzheimer’s disease will experience memory loss, trouble with daily tasks, and other cognitive difficulties. In Alzheimer’s disease, neuroinflammation and inflammation of astroglial and microglial cells occur. Inflammation of these two cells will damage the neurons in the brain, causing the number of synapses to decrease, which impairs cognitive function. With time, the number of neuroinflammations will increase. β-Hairpins peptides are found in proteins; they play an important role in the self-assembly of peptides and proteins. To further explore the functional mechanism of B-bairn, Adam G Kreutzer and James S Nowick assembled the Aβ-hairpins structure. They found that the synthetic Aβ-hairpins structure could produce toxicity to nerve cells, but the effect on astrocytes and microglia was not further explored. In the present study, we isolate and culture the astroglial cell and microglia cultures from newborn mice’s stripped brains. To simulate the beta-hairpin’s environment, we will put different concentrations of protein solutions into the cell cultures. To investigate the effects of the designed β-hairpin peptide on astrocytes and microglia, as well as its potential role in modulating the progression of Alzheimer’s disease, we conducted experiments to examine the expression of inflammation and cellular viability after the addition of the β-hairpin peptide. This paper only provides theoretical experiment design and possible results about the relationship between the β-Hairpins peptides and the inflammation process of astroglial and microglial cells, which needs further research in the pathology of atherosclerosis. It also provided the possibility that β-hairpin peptides regulate Alzheimer’s disease and provided the chance to understand the molecular basis of amyloid diseases.