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Basic Science and Pathogenesis.

Abdallah M Eteleeb1

  • 1Washington University in St. Louis, St. Louis, MO, USA.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 24, 2025
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Summary
This summary is machine-generated.

Long noncoding RNAs (lncRNAs) are linked to worse cognitive function in Alzheimer's disease (AD). A specific lncRNA, WCFAL1, may regulate microglial activity in AD progression.

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Area of Science:

  • Neuroscience
  • Genomics
  • Molecular Biology

Background:

  • Long noncoding RNAs (lncRNAs) are implicated in Alzheimer's disease (AD) pathogenesis.
  • Their specific roles in cognitive decline are not fully understood.
  • This study investigates lncRNAs in AD using multi-omics and machine learning.

Purpose of the Study:

  • To identify lncRNAs associated with cognitive decline in Alzheimer's disease.
  • To elucidate the molecular mechanisms underlying lncRNA involvement in AD.
  • To integrate multi-omics data for a comprehensive understanding of AD pathology.

Main Methods:

  • Machine learning analysis of multi-modal omics data from cortical regions (parietal cortex, dorsolateral prefrontal cortex, parahippocampal gyrus).
  • Identification of protein-coding genes and their interactions with dysregulated lncRNAs via gene regulatory networks, co-expression, and protein-protein interaction analyses.
  • Gene set enrichment and pathway analyses to explore lncRNA regulatory roles.

Main Results:

  • Multi-omics integration revealed an AD molecular profile associated with worse cognition, faster progression, and neurodegeneration.
  • 177 dysregulated lncRNAs, termed WCFALs (Worse Cognitive Function Associated lncRNAs), were identified across cohorts.
  • WCFAL1, the most upregulated lncRNA, strongly correlated with worse cognitive profiles and FOXN3, a microglial regulator, and interacted with SIN3A, linked to amyloid-beta.

Conclusions:

  • lncRNAs are linked to worse cognitive function in Alzheimer's disease.
  • WCFAL1 is a key lncRNA potentially regulating microglial activity via FOXN3 or the FOXN3-SIN3A pathway.
  • Further experimental validation of WCFAL1's function is warranted.