Nature: The study reveals the mechanisms by which Alzheimer's occurs.

September 3, 2020 // --- Alzheimer's disease is a neurodegenerative disease characterized by the accumulation of beta amyloid protein lumps in the brain.
to reveal the causes of these lumps, known as plaques, and what role they play in disease progression, is currently a hot topic of research in this area and is critical to the development of prevention and treatment strategies.
recent study found that beta-amyloid has antiviral and antibacterial properties, suggesting a possible link between the immune response to infection and the development of Alzheimer's disease.
(Photo: www.pixabay.com) Chemical biologists at the Sloan Kettering Institute have now found clear evidence of a link: a protein called IFITM3 is involved in the immune response to pathogens and plays a key role in the accumulation of beta amyloid in plaques.
we know that the immune system works in Alzheimer's disease, for example, by helping to remove beta-amyloid plaques from the brain," said Yueming Li, a chemical biologist at SKI and lead author of the study.
but this is the first direct evidence that the immune response promotes the production of beta-amyloid plaques.
in a paper published September 2 in the journal nature, the authors and others show that IFITM3 alters the enzyme activity of the gamma-secretion enzyme, which is usually responsible for cutting pregenital proteins into fragments of beta-amyloid protein.
they found that removing IFITM3 reduced the activity of gamma-secretion enzymes, thereby reducing the number of amyloid plaques formed in mouse models of the disease.
or brain inflammation has become an important topic in Alzheimer's research.
inflammatory markers, such as some called cytokines, are highly expressed in mouse models of Alzheimer's disease and in the brains of patients with Alzheimer's disease.
the first time the study has established a direct link between inflammation and plaque development through IFETM3.
IFITM3 began by invading viruses and bacteria in response to the activation of the immune system.
new research suggests that IFITM3 directly contributes to plaque formation, meaning that viral and bacterial infections may increase the risk of developing Alzheimer's disease.
, the authors and others found that IFITM3 levels in human brain samples were associated with levels of certain viral infections, gamma-secretase activity, and the production of beta-amyloid proteins.
researchers found that age was the number one risk factor for Alzheimer's disease, with levels of inflammatory markers and IFITM3 increasing with age.
they also found that IFITM3 levels were relatively high in patients with advanced Alzheimer's disease, meaning that IFITM3 could be used as a biomarker to identify some patients who might benefit from treatments for IFITM3.
the researchers' next project is to study how IFIDM3 interacts with gamma-secretase at the molecular and atomic levels and how it is involved in neuroinstatics in animal models.
they will also explore IFITM3 as a biomarker of the disease and as a potential target for new drugs designed to treat the disease.
(bioon.com) Source: Study links to Alzheimer's disease development Source: Hur, J., Frost, G.R., Wu, X. et al. The innate immunity protein IFITM3 modulates s-secretase in Alzheimer's disease. Nature (2020). doi.org/10.1038/s41586-020-2681-2.