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

2.50
Hdl Handle:
http://hdl.handle.net/11287/620421
Title:
ANK1 is up-regulated in laser captured microglia in Alzheimer's brain; the importance of addressing cellular heterogeneity.
Authors:
Mastroeni, D.; Sekar, S.; Nolz, J.; Delvaux, E.; Lunnon, K.; Mill, Jonathan; Liang, W. S.; Coleman, P. D.
Abstract:
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.
Citation:
ANK1 is up-regulated in laser captured microglia in Alzheimer's brain; the importance of addressing cellular heterogeneity. 2017, 12 (7):e0177814 PLoS ONE
Publisher:
PLoS One
Journal:
PloS one
Issue Date:
Jul-2017
URI:
http://hdl.handle.net/11287/620421
DOI:
10.1371/journal.pone.0177814
PubMed ID:
28700589
Additional Links:
http://dx.plos.org/10.1371/journal.pone.0177814
Note:
This article is freely available via Open Access. Click on the Additional Link above to access the full-text via the publisher's site.
Type:
Journal Article
Language:
en
ISSN:
1932-6203
Appears in Collections:
Honorary contracts publications; 2017 RD&E publications

Full metadata record

DC FieldValue Language
dc.contributor.authorMastroeni, D.en
dc.contributor.authorSekar, S.en
dc.contributor.authorNolz, J.en
dc.contributor.authorDelvaux, E.en
dc.contributor.authorLunnon, K.en
dc.contributor.authorMill, Jonathanen
dc.contributor.authorLiang, W. S.en
dc.contributor.authorColeman, P. D.en
dc.date.accessioned2017-10-04T13:22:31Z-
dc.date.available2017-10-04T13:22:31Z-
dc.date.issued2017-07-
dc.identifier.citationANK1 is up-regulated in laser captured microglia in Alzheimer's brain; the importance of addressing cellular heterogeneity. 2017, 12 (7):e0177814 PLoS ONEen
dc.identifier.issn1932-6203-
dc.identifier.pmid28700589-
dc.identifier.doi10.1371/journal.pone.0177814-
dc.identifier.urihttp://hdl.handle.net/11287/620421-
dc.description.abstractRecent 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.en
dc.language.isoenen
dc.publisherPLoS Oneen
dc.relation.urlhttp://dx.plos.org/10.1371/journal.pone.0177814en
dc.rightsArchived with thanks to PloS oneen
dc.subjectWessex Classification Subject Headings::Oncology. Pathology.::Geneticsen
dc.titleANK1 is up-regulated in laser captured microglia in Alzheimer's brain; the importance of addressing cellular heterogeneity.en
dc.typeJournal Articleen
dc.identifier.journalPloS oneen
dc.description.noteThis article is freely available via Open Access. Click on the Additional Link above to access the full-text via the publisher's site.en
dc.type.versionPublisheden

Related articles on PubMed

All Items in RD&E Research Repository are protected by copyright, with all rights reserved, unless otherwise indicated.