Researchers at the University of Kentucky have completed a study that revealed differences in the way neuroinflammation, considered a key component of Alzheimer’s disease, is expressed in different subsets of patients, in particular people with Down syndrome.
Previous studies show that people with Down syndrome have a third copy of Chromosome 21, and that chromosome is the same one responsible for the production of a molecule called amyloid precursor protein. Amyloid overproduction can lead to brain plaques that are a cardinal feature of Alzheimer’s, so it is not surprising that nearly 100 percent of people with Down syndrome develop Alzheimer’s disease pathology in their brain by the time they are 40.
The team state that people develop Alzheimer’s disease at different ages, but it’s typically in their 60s, 70s, or 80s. They go on to add that it’s a little easier to study Alzheimer’s disease in Down syndrome because of the predictability of the age when adults with Down syndrome develop signs of the disease.
The current study used brain autopsy tissue from a group of people to determine differences in the way neuroinflammation was expressed in people with Down syndrome. The samples came from people with Down syndrome with Alzheimer’s, people with Alzheimer’s alone, and healthy controls.
Previous studies from the team identified different types of inflammation in Alzheimer’s brains, two families of inflammatory markers, called M1 and M2a, were each present to varying degrees in the sample population representing early Alzheimer’s cases, indicating a notable level of heterogeneity in the way the Alzheimer’s disease process begins in the brain. But in the late-stage Alzheimer’s cases, there was a high degree of homogeneity with high levels of the markers M1, M2 and M2c.
In the current study the team found that the inflammatory response in Down syndrome/Alzheimer’s disease brain tissue was significantly greater than that in tissue from Alzheimer’s disease patients. Furthermore, there was an elevated level of markers for M2b, that was not replicated in tissue from sporadic Alzheimer’s cases. In other words, Alzheimer’s disease in the Down syndrome brain had a very different neuroinflammatory profile than Alzheimer’s disease in people without Down syndrome.
The researchers note that it has been generally assumed that Alzheimer’s disease presents the same way in people with Down syndrome as it does in people without Down syndrome, however, their work demonstrates that this is not the case. They go on to add that this will have important implications for the study of Alzheimer’s treatments, as some treatments might be effective with people without Down syndrome and not those with Down syndrome.
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