Amyloid Plaques Containing Nucleic Acids Drive Neuroinflammation in Alzheimer ' s Disease

Alzheimer's disease is characterized by the presence of protein aggregates in the brain. These are misfolded and altered versions of proteins that can act as seeds for solid deposits to form and spread in the brain. These deposits are surrounded by a halo of toxic biochemistry that harms and eventually kills neurons. Amyloid-β aggregates are present in the early stages of the condition, while tau aggregates cause much greater harm and cell death in the later stages. Alzheimer's disease is also an inflammatory condition, however, in which chronic inflammation and altered behavior of the central nervous system immune cells known as microglia is clearly very influential. The interaction between amyloid-β, tau, and inflammation is somewhat debated. One view is that early amyloid-β aggregation causes microglia to become dysfunction and inflammatory, and this behavior generates an environment of chronic inflammation that results in tau aggregation. Alternatively, amyloid-β accumulation may just be a side-effect of persistent infections that produce chronic inflammation in the brain. Both of these options might be true to varying degrees in different patients. It is quite challenging to pick apart the mechanisms of early Alzheimer's in humans, as it isn't feasible to open up large numbers of living brains to take a look at their biochemistry. Today's research materials add support for the more complex picture of differing contributions and interactions of amyloid-Î...
Source: Fight Aging! - Category: Research Authors: Tags: Medicine, Biotech, Research Source Type: blogs