The formation and deposition of the -amyloid peptide (A) are largely thought to be responsible for the development of Alzheimer's disease (AD). Researchers have been perplexed by the sluggish to nonexistent association between the degree of clinical dementia and the amount of neuritic plaque disease in the human brainfor a long time. This question has been resolved thanks to recentdevelopments in our knowledge of the origins of amyloid disease.The solubility of A and the amount of A in various pools may nowbe more directly tied to disease state, according to substantialevidence. The make-up of these pools of A reflects variouspopulations of amyloid deposits and is clearly correlated with thepatient's clinical condition. Using imaging methods, such as novelamyloid imaging agents based on the chemical makeup of histologydyes, it is now possible to monitor the development of the diseasein a living patient while also monitoring the amyloid pathology. It'sinteresting that these methods show that the A deposited in ADdiffers from that discovered in animal models. In general, depositedA does not exhibit the same physical and biochemical propertiesas the amyloid observed in AD and is more readily removed fromthe brain in animal studies. Important questions about the creationand evaluation of potential medicinal agents are brought up by this.
Keywords: Amyloid, β-Amyloid precursor protein, Aβ, Oligomer, Fibril