Evidence for Bacterial DNA to Promote Tau Aggregation in Neurodegeneration

The field of Alzheimer's disease research is in the midst of a slow-moving and consequential debate over the role of infection in the development of the condition. The fundamental question is this: in the absence of genetic variants that raise risk, why do only some people progress to full blown Alzheimer's disease? The presence - in only some people - of sufficient degrees of persistent infection is one possible answer to that question. Candidates include herpesviruses, oral bacteria such as P. gingivalis, lyme disease spirochetes, and others.

Alzheimer's is a condition characterized by amyloid-β aggregation in its early stages and tau aggregation in its later, more severe stages. The classic amyloid cascade view of the condition is that amyloid-β aggregation sets the stage for immune dysfunction and chronic inflammation leading to tau aggregation. The debate over whether or not persistent infection instead lies at the root of the condition has so far largely focused firstly on amyloid-β as an anti-microbial peptide, a part of the innate immune system that may be upregulated by infection, and secondly on the chronic inflammation that results from infection, as inflammation in the brain clearly strongly drives tau pathology.

Here, however, researchers offer evidence for the presence of bacterial DNA to accelerate the processes of tau aggregation through mechanisms independent of inflammation. Some forms of bacterial DNA may help to seed the aggregates of tau ...

Source: Fight Aging! - February 21, 2020 Category: Research Authors: Reason Tags: Medicine, Biotech, Research Source Type: blogs