| Literature DB >> 32702314 |
Wei-Ting Chen1, Ashley Lu1, Katleen Craessaerts1, Benjamin Pavie2, Carlo Sala Frigerio3, Nikky Corthout2, Xiaoyan Qian4, Jana Laláková4, Malte Kühnemund4, Iryna Voytyuk1, Leen Wolfs1, Renzo Mancuso1, Evgenia Salta1, Sriram Balusu1, An Snellinx1, Sebastian Munck2, Aleksandra Jurek5, Jose Fernandez Navarro5, Takaomi C Saido6, Inge Huitinga7, Joakim Lundeberg5, Mark Fiers8, Bart De Strooper9.
Abstract
Although complex inflammatory-like alterations are observed around the amyloid plaques of Alzheimer's disease (AD), little is known about the molecular changes and cellular interactions that characterize this response. We investigate here, in an AD mouse model, the transcriptional changes occurring in tissue domains in a 100-μm diameter around amyloid plaques using spatial transcriptomics. We demonstrate early alterations in a gene co-expression network enriched for myelin and oligodendrocyte genes (OLIGs), whereas a multicellular gene co-expression network of plaque-induced genes (PIGs) involving the complement system, oxidative stress, lysosomes, and inflammation is prominent in the later phase of the disease. We confirm the majority of the observed alterations at the cellular level using in situ sequencing on mouse and human brain sections. Genome-wide spatial transcriptomics analysis provides an unprecedented approach to untangle the dysregulated cellular network in the vicinity of pathogenic hallmarks of AD and other brain diseases.Entities:
Keywords: Alzheimer’s disease; amyloid plaque; astrocyte; cellular phase; complement cascade; in situ sequencing; microglia; myelination; oligodendrocyte; spatial transcriptomics
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Year: 2020 PMID: 32702314 DOI: 10.1016/j.cell.2020.06.038
Source DB: PubMed Journal: Cell ISSN: 0092-8674 Impact factor: 41.582