ASC Specks in the Inflammatory Microglial Response to Amyloid- β Aggregation in Alzheimer ' s Disease

The Alzheimer's disease research community is nowadays ever more strongly considering chronic inflammation in the brain as a vital part of the progression of the condition. In the amyloid cascade hypothesis, a slow aggregation of amyloid-β over decades (for reasons that are debated) causes ever greater inflammatory dysfunction in microglia, the immune cells of the brain responsible for clearing up metabolic waste such as protein aggregates. That inflammation in turn sets the stage for tau aggregation to take place to a significant degree, causing cell death and severe neural dysfunction. Today's open access research is an example of the sort of work taking place to better understand how amyloid-β interacts with microglia to produce the outcome of chronic inflammation. In principle at least, a better understanding usually leads to new targets for the development of drugs that can interfere in the process. A great deal of hypothesizing takes place among Alzheimer's researchers. The animal models are highly artificial, and thus prone to misleading results, there is a great deal of dissatisfaction with the decades-long relentless focus on amyloid-β, and it is very costly to prove any particular point using human data and human patients. Theorizing is thus a great deal easier than validating any given hypothesis, and as a result there are are numerous variations on the basic idea that chronic inflammation is an important part of the progression of Alzheimer's dise...
Source: Fight Aging! - Category: Research Authors: Tags: Medicine, Biotech, Research Source Type: blogs