Researchers and pharma companies have tried to attack this disease by reducing amyloid plaques, but inflammation may be the real culprit.
To investigate whether IL-1 might play a role in Lewy body pathology seen in Alzheimer's, we tested the role of IL-1 in alpha-synuclein fiber production using three methods: in tissue culture, in IL-1-pellet implanted rat brains, and in brain slices from Alzheimer’s patients. All three methods gave the same results, showing that IL-1 overexpression was associated with increased production of alpha-synuclein
http://the-scientist.com/2011/09/01/what-causes-alzheimers/
A nice link IL-1 and spirochetes:
Interleukin- 1 gene polymorphisms as assessed in a 10-year study of patients with early-onset periodontitis.
http://www.ncbi.nlm.nih.gov/pubmed/17575917 and
Salivary interleukin-1beta concentration and the presence of multiple pathogens in periodontitis.
Thanks for the links. I appreciate them. Dr. Miklossy points out in her paper that these oral spirochetes are capable of triggering the human immune response for their OWN defense. After reading the first paper on inflammation, and it’s involvement, I wonder if that is not part of the AD modality?
A notorious Alzheimer’s disease villain may also be a germ-busting superhero. Amyloid-beta gums up the brains of people with Alzheimer’s but also takes out dangerous brain invaders, scientists report May 25 in Science Translational Medicine.
The next step is to see whether pathogens are entombed in A-beta plaques in the human brain, Tanzi says. “Now it’s time to start looking for them in patients.” To start, he and colleagues have just begun a project to catalog the collection of microbes in healthy brains and brains with Alzheimer’s.
Finding a strong link between pathogens and Alzheimer’s could suggest new ways to prevent the disease, Tanzi says. Vaccines that fight infections, for instance, might be one way to prevent A-beta pileup.
https://www.sciencenews.org/article/alzheimer%E2%80%99s-culprit-may-fight-other-diseases
Despite the blood-brain barrier’s efforts to keep them out, microbes – including yeast, chlamydia, spirochetes and herpes – manage to infect the brain, as they do every other organ.
Tanzi, co-corresponding author Robert Moir and their team first started to wonder whether plaques might have an immune function when they noted structural similarities between beta-amyloid and other antimicrobial peptides, and had previously published in vitro data supporting the idea that beta-amyloid had a role in innate immunity.
In their current experiments, published in the May 27, 2016, issue of Science, the team showed that high levels of amyloid beta protected mice against brain infections with the bacterium Salmonella typhimurium, and transgenic roundworms expressing amyloid beta were less susceptible to fungal infections.
http://www.bioworld.com/content/amyloid-plaques-%E2%80%98entomb%E2%80%99-microbes-immune-defense-0