Tshetiz Dahal*
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 brain for a long time. This question has been resolved thanks to recent developments in our knowledge of the origins of amyloid disease. The solubility of A and the amount of A in various pools may now be more directly tied to disease state, according to substantial evidence. The make-up of these pools of A reflects various populations of amyloid deposits and is clearly correlated with the patient's clinical condition. Using imaging methods, such as novel amyloid imaging agents based on the chemical makeup of histology dyes, it is now possible to monitor the development of the disease in a living patient while also monitoring the amyloid pathology. It's interesting that these methods show that the A deposited in AD differs from that discovered in animal models. In general, deposited A does not exhibit the same physical and biochemical properties as the amyloid observed in AD and is more readily removed from the brain in animal studies. Important questions about the creation and evaluation of potential medicinal agents are brought up by this.
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