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Alzheimer's disease, as a neurodegenerative disease, has great unfinished medical needs.
there has been a lack of effective treatments for the disease.
many clinical trials over the past decade or so have largely failed.
these results, scientists are also debating what role beta amyloid plays in Alzheimer's disease.
recent years, there has been a new understanding of the pathology of Alzheimer's disease.
studies have found that beta amyloid has antiviral, or antimicrobial, properties that indicate an immune response to infection that may be linked to the onset of Alzheimer's disease.
although the innate immune response is associated with the disease, it is not known how activation of the immune system affects the production of beta amyloid proteins.
in this study, scientists found a protein called interferon-induced transmeral protein (IFITM3) and confirmed that it is part of the gamma secretion enzyme complex and regulates the activity of gamma secretion enzymes.
in the pathological occurrence of Alzheimer's disease, gamma secretion enzymes are known to be able to cut the pregenes of amyloid proteins together with other enzymes to produce beta amyloid proteins.
the latter can form pathological protein deposits of Alzheimer's disease.
the role of gamma secretion enzymes (Photo Source: Supplied) The researchers found that the level of expression of IFITM3 also increased with age.
, ifITM3 levels of expression also increased in mouse models with Alzheimer's disease.
so what does IFITM3 have to do with the production of beta amyloid protein? To answer this question, the researchers knocked out IFITM3 in mouse models and found that although levels of the gamma secretion enzyme complex did not decrease compared to wild controls, their activity decreased significantly and their ability to produce two beta amyloid proteins decreased by 15.3% and 24.3%, respectively.
the removal of IFITM3, the ability of the enzyme to produce beta amyloid protein decreased (Photo source: Reference 1) The scientists concluded that the emergence of beta amyloid protein due to aging was at least partly due to an increase in IFITM3 levels.
other analyses have also shown that IFITM3 levels do show a strong positive correlation with the activity of gamma secretion enzymes.
based on these findings, the researchers built a pathological model in which inflammatory cytokines induce the expression of IFITM3 in neurons and astrological glial cells after infection with bacteria or viruses.
the latter combines gamma secretion enzymes to increase its activity and produce more beta amyloid proteins.
We know that the immune system plays a role in the onset of Alzheimer's disease, such as by removing beta amyloid protein from the brain," commented professor Li Yuming, co-author of the study.
protein is a key feature of Alzheimer's disease.
believes that as more and more evidence links inflammatory responses to Alzheimer's disease, so will our understanding of the disease.
we look forward to scientists to find an early way to overcome Alzheimer's disease for the benefit of mankind! Re-references: Hur, J., Frost, G.R., Wu, X. et al. The innate immunity protein IFITM3 modulates s-secretase in Alzheimer's disease. Nature (2020).MSK study links to Alzheimer's disease development Retrieved September 2, 2020, from s3, Gertsik N, Chiu D and Li Y-M (2014) Complex regulation of the s-secretase: from the obligatory to modulatory subunits. Front. Aging Neurosci. 6:342. doi: 10.3389/fnagi.2014.00342.