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Author Spotlight: Exploring Sex-Specific Glial Signatures and Therapeutic Leads for Alzheimer&#39;s Disease
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Exploring Gene Expression Patterns in Alzheimer's Disease Using a Human Microarray Data Meta-Analysis.

Eleni Dermitzaki1,2,3, Vasileios L Zogopoulos1,2, Apostolos Malatras4

  • 1Center of Systems Biology, Biomedical Research Foundation, Academy of Athens, 11527 Athens, Greece.

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|February 26, 2026
PubMed
Summary
This summary is machine-generated.

This study analyzed gene expression in Alzheimer's disease (AD) brains, identifying key differences. Findings reveal immune responses and inflammation in AD, contrasting with synaptic pathway collapse, offering potential diagnostic and prognostic biomarkers.

Keywords:
Tau proteinagingamyloid betabraindementiadifferential gene expressionneurodegenerationrobust multichip analysissystems biologytranscriptomics

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Area of Science:

  • Neuroscience and Genetics
  • Molecular Biology

Background:

  • Alzheimer's disease (AD) is a leading neurodegenerative disorder, with aging as the primary risk factor.
  • The escalating global elderly population correlates with a rising prevalence of AD.
  • AD pathology begins years before symptom onset, underscoring the need for early diagnosis and prognosis.

Purpose of the Study:

  • To identify differentially expressed genes (DEGs) between Alzheimer's disease and healthy brains.
  • To discover genes with potential as risk factors, diagnostic, prognostic, or pharmacological biomarkers for AD.

Main Methods:

  • Systematic meta-analysis of microarray datasets from public repositories, adhering to PRISMA 2020 guidelines.
  • Quality control, data normalization, and Mosteller-Bush meta-analysis to combine DEG lists from eight studies.
  • Enrichment analysis of statistically significant DEGs using an adjusted p-value cut-off of 0.001.

Main Results:

  • A combined list of 4218 DEGs was identified between AD and healthy brains.
  • 1944 DEGs were up-regulated, enriched for immune response and inflammation-related processes.
  • 2274 DEGs were down-regulated, enriched for synapse-related pathways and neuronal signaling.

Conclusions:

  • Alzheimer's disease exhibits a distinct transcriptomic profile characterized by heightened immune activity.
  • A significant collapse in synaptic and neuronal signaling pathways is evident in AD brains.
  • Identified DEGs offer potential for early AD diagnosis, prognosis, and therapeutic target development.