The consciousness of the brain is the basis of all human activities, if the brain activity disorder or stop, human life will be seriously threatened. Alzheimer's disease (AD) is a relatively common brain disease characterized by progressive memory loss and cognitive impairment. It is not yet clear what brain activity causes Alzheimer's, but the production and accumulation of beta-amyloid has long been thought to be an important factor.
Aβis encoded by the APP produced through A series of hydrolase enzyme, the APP is Aβprecursor protein, full name is the amyloid precursor protein, APP across the membrane in the process of production there are 2 hydrolysis ways, which does not produce AD the starch source way and generate Aβsource of starch way, in the first article in hydrolysis pathways, APP proteolytic and secretion after α-secretes enzyme action, produce soluble α- APPs and released into the extracellular, leave the APP alpha CTF at the same time, this process destroys A complete structure of beta, no neurotoxicity, this process is known as the amyloid production means, under normal circumstances, This metabolic pathway is dominant. Aβis produced by the starch source pathway. APP, under the action ofβ-secretase, secretes soluble beta-apps and c-terminal fragments (β-CTF) from the n-terminal of Aβregion, and then continues to cleave by γ-secretase, producing a series of Aβand AICD of different lengths. In this process, if the balance between the production and clearance of Aβis broken, abnormal deposition of Aβ in the cerebral cortex will be caused, which will lead to synaptic damage and degeneration of neurons.
So what exactly is the relationship between Aβand AD? The pathogenesis of AD is very complex. At present, there is no clear explanation for the pathogenesis of AD, and many theories are in the hypothesis stage. The dominant hypothesis is the Aβ hypothesis. This hypothesis holds that
Aβis the initial factor that induces AD. Large amount of production, accumulation and deposition of Aβwill have a direct toxic effect on neurons, and also induce inflammation in the brain, which will lead to the production and deterioration of AD disease. In recent years, researchers have focused on the formation, aggregation and clearance of Aβ.