ANK1 Expression Change May Cause Neuroinflammation

ANK1 Expression Change May Cause Neuroinflammation
Expression of the protein ANK1 (ankyrin repeat domain-containing protein) is four fold higher in the microglia of patients with Alzheimer’s disease (AD). Microglia are a type of immune cell found in the brain and key regulators of the inflammatory cascade typified in early Alzheimer's development. ANK1 previously has been identified as a potential risk factor for the development of AD. Researchers at Arizona State University determined expression of ANK1 in three different types of brain cells, microglia, astrocytes, and neurons, using a technique called laser capture microdissection. These cells were obtained from the hippocampus part of the brain of patients with AD. The hippocampus is the area that is responsible for both short-term and long-term memory. Results from this study were published in an article titled, “ANK1 is up-regulated in laser captured microglia in Alzheimer’s brain; the importance of addressing cellular heterogeneity,” in the journal PloS One. The study showed that ANK1 expression in the hippocampus is significantly increased by four fold in the microglial cells, but not in the neurons or astrocytes from the same individuals. "Although previous genetic and epigenetic-wide association studies had shown a significant association between ANK1 and AD, they were unable to identify the class of cells that may be responsible for such association because of the use of brain homogenates. Here, we provide evidence that microglia are the source of the previously observed differential expression patterns in the ANK1 gene in Alzheimer's disease," said Dr.
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One comment

  1. Dante J Marciani says:

    It is interesting how inflammation is more and more becoming the villain of Alzheimer’s disease. Yet, most of the failed studies and many of the still ongoing use effective pro-inflammatory agents, which explains the customary failures in the Alzheimer’s immunotherapy approach, besides of trying to treat the disease when it is obvious beyond hope. Yet, for reasons difficult to understand, Alzheimer’s immunotherapy scientists refuse to use new anti-inflammatory immunomodulators.

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