Tackling Amyloid- β Oligomers by Interfering in Specific Interactions Necessary to Protein Aggregation

The present consensus on the the development of Alzheimer's disease is that it starts with the accumulation of amyloid-β, though there are many competing theories as to why only some people exhibit this problem to a great enough degree to produce pathology. The biochemistry of oligomers supporting amyloid-β causes sufficient disarray in brain metabolism to set the stage for neuroinflammation, malfunction of immune cells in the brain, and aggregation of altered forms of tau protein into neurofibrillary tangles that cause most of the damage and cell death in the later stages of the condition. The failure to improve outcomes via attempts to remove amyloid-β from the brains of Alzheimer's patients may be a case of too little, too late, but there is still good reason to remove amyloid-β. Doing so early enough and efficiently enough should prevent the later stages of the condition from developing at all. The most modern approach to drug development, built atop greatly improved capacities in computation and associated modeling of protein structures and interactions, is to find points of intervention through a greater understanding of how proteins interact with one another, in detail, and how those interactions pertain to disease processes. Researchers can then rationally design molecules that (a) interfere at a vulnerable and highly specific point in a desired interaction and (b) due to this specificity are safe enough for clinical use, as they cause only limited disrupti...
Source: Fight Aging! - Category: Research Authors: Tags: Medicine, Biotech, Research Source Type: blogs