Alzheimer’s disease is a neurodegenerative condition that is characterized by the buildup of clumps of beta-amyloid protein in the brain.
Exactly what causes these clumps, known as plaques, and what role they play in disease progression is an active area of research important for developing prevention and treatment strategies.
Recent studies have found that beta-amyloid has antiviral and antimicrobial properties, suggesting a possible link between the immune response against infections and the development of Alzheimer’s disease.
In a recent study from the Sloan Kettering Institute, researchers discovered clear evidence of this link: A protein called IFITM3 that is involved in the immune response to pathogens also plays a key role in the accumulation of beta-amyloid in plaques.
Scientists have known that the immune system plays a role in Alzheimer’s disease — for example, it helps to clean up beta-amyloid plaques in the brain.
But this is the first direct evidence that immune response contributes to the production of beta-amyloid plaques — the defining feature of Alzheimer’s disease.
In the study, the team found that IFITM3 alters the activity of an enzyme called gamma-secretase, which chops up precursor proteins into the fragments of beta-amyloid that make up plaques.
They found that removing IFITM3 decreased the activity of the gamma-secretase enzyme and, as a result, reduced the number of amyloid plaques that formed in a mouse model of the disease.
Neuroinflammation, or inflammation in the brain, has emerged as an important line of inquiry in Alzheimer’s disease research.
Markers of inflammation, such as certain immune molecules called cytokines, are boosted in Alzheimer’s disease mouse models and in the brains of people with Alzheimer’s disease.
This study is the first to provide a direct link between this inflammation and plaque development — by way of IFITM3.
The team found age is the number one risk factor for Alzheimer’s, and the levels of both inflammatory markers and IFITM3 increased with advancing age in mice.
They also discovered that IFITM3 is increased in a subset of late-onset Alzheimer’s patients, meaning that IFITM3 could potentially be used as a biomarker to identify a subset of patients who might benefit from therapies targeted against IFITM3.
They will explore IFITM3 as a biomarker for Alzheimer’s disease and as a potential target for new drugs designed to treat it.
If you care about Alzheimer’s disease, please read studies about a noninvasive treatment for Alzheimer’s disease and findings of subconscious changes in movement may predict Alzheimer’s disease.
For more information about Alzheimer’s and your health, please see recent studies about these 2 personality traits may protect you from Alzheimer’s disease and more and results showing a new early sign of Alzheimer’s disease.
The study is published in Nature. One author of the study is Yue-Ming Li.
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