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PLoS One. 2017 Jul 12;12(7):e0177814. doi: 10.1371/journal.pone.0177814. eCollection 2017.

ANK1 is up-regulated in laser captured microglia in Alzheimer's brain; the importance of addressing cellular heterogeneity.

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Biodesign, ASU-Banner Biodesign Neurodegenerative Disease Research Center, and School of Life Sciences, Arizona State University, Tempe, AZ, United States of America.
Banner Sun Health Research Institute, 10515 West Santa Fe Drive, Sun City, AZ, United States of America.
Translational Genomics Institute, 445 North Fifth Street, Phoenix, AZ, United States of America.
University of Exeter Medical School, RILD, University of Exeter, Devon, United Kingdom.
Institute of Psychiatry, Psychology and Neuroscience, King's College London, De Crespigny Park, London, United Kingdom.


Recent epigenetic association studies have identified a new gene, ANK1, in the pathogenesis of Alzheimer's disease (AD). Although strong associations were observed, brain homogenates were used to generate the data, introducing complications because of the range of cell types analyzed. In order to address the issue of cellular heterogeneity in homogenate samples we isolated microglial, astrocytes and neurons by laser capture microdissection from CA1 of hippocampus in the same individuals with a clinical and pathological diagnosis of AD and matched control cases. Using this unique RNAseq data set, we show that in the hippocampus, ANK1 is significantly (p<0.0001) up-regulated 4-fold in AD microglia, but not in neurons or astrocytes from the same individuals. These data provide evidence that microglia are the source of ANK1 differential expression previously identified in homogenate samples in AD.

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