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Related Experiment Video

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Meta-Analysis of the Alzheimer's Disease Human Brain Transcriptome and Functional Dissection in Mouse Models.

Ying-Wooi Wan1, Rami Al-Ouran2, Carl G Mangleburg1

  • 1Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030, USA; Jan and Dan Duncan Neurologic Research Institute, Texas Children's Hospital, Houston, TX 77030, USA.

Cell Reports
|July 16, 2020
PubMed
Summary

This study created a human brain gene atlas for Alzheimer's disease (AD), revealing key gene networks and their links to mouse models. Findings offer insights into disease mechanisms and potential therapeutic targets.

Keywords:
Alzheimer's diseaseRNA-seqagingcoexpression analysisdifferential expression analysismeta-analysismouse modelsneuroinflammationtranscriptome

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Area of Science:

  • Neuroscience
  • Genomics
  • Pathology

Background:

  • Alzheimer's disease (AD) pathogenesis involves complex transcriptional changes in the human brain.
  • Understanding these changes is crucial for developing effective disease models and treatments.

Purpose of the Study:

  • To construct a consensus atlas of the human brain transcriptome in Alzheimer's disease (AD).
  • To identify major sources of transcriptional perturbations in AD.
  • To compare human findings with mouse models of neurodegenerative diseases.

Main Methods:

  • Meta-analysis of differential gene expression in 2,114 postmortem human brain samples.
  • Identification of 30 brain coexpression modules across seven brain regions.
  • Comparative analysis of human gene sets with 251 differentially expressed gene sets from mouse models.

Main Results:

  • Thirty brain coexpression modules were identified as major sources of AD transcriptional changes.
  • Human-mouse overlaps revealed distinct responses to amyloid and tau pathology.
  • Age- and sex-dependent expression signatures associated with AD progression were identified.
  • Neuronal and microglial gene modules showed broad overlap with various neurodegenerative disease models and aging.

Conclusions:

  • The study provides a valuable cross-species resource for understanding human brain pathophysiology in AD.
  • Identified transcriptional networks and human-mouse correspondences can inform preclinical AD studies.
  • Specific gene modules implicated in proteostasis were not activated in AD models, suggesting distinct biological pathways.