Today, the journal Nature published an important research paper on Alzheimer's disease online.
team, from Memorial Sloan-Kettering Cancer Center, found that a protein involved in the innate immune response could influence the production of β amyloid, a key pathological protein for Alzheimer's disease.
the agency's press release that the study is the first to show that the immune response promotes the production of this key pathological protein.
alzheimer's disease as a neurodegenerative disease, there is a great deal of unfinished medical needs.
there has been a lack of effective treatments for the disease.
many clinical trials over the past decade or so have mostly failed.
these results, scientists are also β what role amyloid protein plays in Alzheimer's disease.
recent years, new understandings have been made about the pathology of Alzheimer's disease.
studies have found that β amyloid has antiviral, or antimicrobial properties, indicating that an immune response caused by infection 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 β amyloid proteins.
in this study, scientists found a protein called interferon-induced transmeral protein (IFITM3) and confirmed that it is part of the γ secretion enzyme complex and regulates the activity of γ secretion enzymes.
in the pathological occurrence of Alzheimer's disease, γ secretion enzymes are known to be able to cut the pregenes of amyloid, together with other enzymes, to produce β amyloid proteins.
the latter can form pathological protein deposits of Alzheimer's disease.
the γ the secretion of enzymes (Photo Source: Supplied) and 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 β to the production of amyloid protein in the united states? To answer this question, the researchers knocked out IFITM3 in mouse models and found that although levels of γ secretion enzyme complexes did not decrease compared to wild controls, their activity decreased significantly, and their ability to produce two β amyloid proteins decreased by 15.3% and 24.3%, respectively.
the γ secretion enzyme's ability to produce β amyloid protein decreased after the
knock-out (Photo source: Reference 1) Scientists concluded that the emergence of β amyloid proteins 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 γ positive correlation with the activity of 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 γ secretion enzymes to increase its activity and produce β more amyloid proteins.
We know that the immune system plays a role in the onset of Alzheimer's disease, such as it clears β amyloid proteins from the brain," commented study co β-author Professor Li Yuming.
protein is a key feature of Alzheimer's disease.
believes that as more and more evidence links inflammatory responses to Alzheimer's disease, our understanding of the disease will grow.
we look forward to scientists finding an early way to conquer 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 γ-secretase in Alzheimer's disease. Nature (2020). MSK study links to Alzheimer's disease development, Retrieved September 2, 2020, from Gertsik N, Chiu D and Li Y-M (2014) Complex regulation of γ-secretase: from obligatory to modulatory subunits. Front. Aging Neurosci. 6:342. doi: 10.3389/fnagi.2014.00342