A Genome-wide Gene-Expression Analysis and Database in Transgenic Mice during Development of Amyloid or Tau Pathology

被引：210

作者：

Matarin, Mar ^{[1
,3
,4
]}

Salih, Dervis A. ^{[2
]}

Yasvoina, Marina

Cummings, Damian M. ^{[2
]}

Guelfi, Sebastian ^{[3
,4
]}

Liu, Wenfei ^{[2
]}

Solim, Muzammil A. Nahaboo ^{[2
,7
]}

Moens, Thomas G. ^{[2
]}

Paublete, Rocio Moreno ^{[2
]}

Ali, Shabinah S. ^{[2
]}

Perona, Marina ^{[1
]}

Desai, Roshni ^{[7
]}

Smith, Kenneth J. ^{[7
]}

Latcham, Judy ^{[5
]}

Fulleylove, Michael ^{[5
]}

Richardson, Jill C. ^{[6
]}

Hardy, John ^{[3
,4
]}

Edwards, Frances A. ^{[2
]}

机构：

[1] Inst Neurol, Dept Clin & Expt Epilepsy, London WC1N 3BG, England

[2] UCL, Dept Neurosci Phys & Pharmacol, London WC1E 6BT, England

[3] UCL, Inst Neurol, Reta Lila Res Labs, London WC1N 1PJ, England

[4] UCL, Inst Neurol, Dept Mol Neurosci, London WC1N 1PJ, England

[5] GlaxoSmithKline R&D, Dept Lab Anim Sci, Stevenage SG1 2NY, Herts, England

[6] GlaxoSmithKline R&D, Neurosci Therapeut Area, Stevenage SG1 2NY, Herts, England

[7] UCL, Inst Neurol, Dept Neuroinflammat, London WC1N 3BG, England

来源：

CELL REPORTS | 2015年 / 10卷 / 04期

基金：

英国医学研究理事会;

关键词：

ALZHEIMERS-DISEASE; PRECURSOR PROTEIN; MOUSE MODEL; APP; DEPOSITION; PROFILES; NETWORKS; NEURONS; BRAINS; TREM2;

D O I：

10.1016/j.celrep.2014.12.041

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

We provide microarray data comparing genome-wide differential expression and pathology throughout life in four lines of "amyloid'' transgenic mice (mutant human APP, PSEN1, or APP/PSEN1) and "TAU'' transgenic mice (mutant human MAPT gene). Microarray data were validated by qPCR and by comparison to human studies, including genome-wide association study (GWAS) hits. Immune gene expression correlated tightly with plaques whereas synaptic genes correlated negatively with neurofibrillary tangles. Network analysis of immune gene modules revealed six hub genes in hippocampus of amyloid mice, four in common with cortex. The hippocampal network in TAU mice was similar except that Trem2 had hub status only in amyloid mice. The cortical network of TAU mice was entirely different with more hub genes and few in common with the other networks, suggesting reasons for specificity of cortical dysfunction in FTDP17. This Resource opens up many areas for investigation.

引用

页码：633 / 644

页数：12

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