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Text . . Le yuan Alzheimer's disease (AD) is a neurodegenerative disease in which β-amyloid proteins accumulate in the brain.
reveal the causes of these plaques and their role in disease progress is critical to developing strategies for the prevention and treatment of Alzheimer's disease.
The growing body of research suggests that β-amyloid proteins have antimicrobial and antiviral activity as part of the brain's innate immune response, suggesting a possible link between pathogen-inspired immune responses and the development of Alzheimer's disease.
in a paper published September 2 in Nature, Professor Li Yuming of the Sloan Catherine Cancer Research Center found clear evidence of this link: interferon-induced transmembrane protein 3 (IFITM3) is involved in the immune response to pathogens and alters the activity of γ-secretase, an enzyme that cut presuppressin into β-amyloid fragments.
and knocking out IFITM3 reduces the activity of γ-secretion enzymes, thereby reducing the number of amyloid plaques forming in Alzheimer's mouse models.
: NatureIFITM3 has a wide range of antiviral activity and is the first line of defense against infection.
addition, IFITM3 is γ of the two-secretion enzyme complex.
researchers found that IFITM3 expression levels were associated with γ-secretase activity, and that knocking down or knocking out IFITM3 reduced the production of γ-secretase activity and β-amyloid protein.
note that excessive expression of IFT3 in gene knock-out cell line restores the γ of the gene-secretion enzyme.
the effects of IFITM3 on γ-secretase activity (Source: Nature) After analyzing a large number of mouse brain samples, the researchers found that aging was the number one risk factor for Alzheimer's disease, with levels of inflammatory markers and IFITM3 increasing with age Increased growth, and an increase in IFITM3 expression was observed in brain samples of some patients with late-onset Alzheimer's disease (LOAD), meaning that IFITM3 may be a biomarker used to identify patients who may benefit from IFITM3 targeted therapy.
the association of IFITM3 with γ-secretase complexes in the human brain (source: Nature) the mechanisms of inflammation and Alzheimer's disease revealed in this study.
caused by viral infection or aging can lead to elevated IFITM3 levels, which increases γ-secretion enzyme activity and leads to the production of human β-amyloid proteins.
The association between congenital immunity and the production of β-amyloid protein and the risk of Alzheimer's disease (Source: Nature) In general, this study identified IFITM3 as a new type of γ-secretase-regulating protein and established a direct link between inflammation and the development of Alzheimer's plaques for the first time.
researchers' next research project is to explore how IFIDM3 interacts with γ-secretase at the molecular and atomic levels and how IFAT3 is involved in neuroinstatic inflammation in animal models.
, the researchers will also explore IFITM3 as a biomarker for Alzheimer's disease and a potential target for new drugs.
: 1 s Hur, J. et al. The innate immunity protein IFITM3 modulates γ-secretase in Alzheimer's disease. Nature (2020)2 s links to Alzheimer's disease development (Source: MedicalXpress)