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Basic Science and Pathogenesis.

Julianna N Brutman1, Marissa J de Leon1, Samuel Smukowski1

  • 1University of Washington, Seattle, WA, USA.

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Summary
This summary is machine-generated.

Investigating presenilin 2 (PSEN2) 3' untranslated region (3'UTR) isoforms in Alzheimer's disease (AD) revealed differential localization and miRNA regulation. Understanding PSEN2 3'UTR isoform function is crucial for advancing AD research.

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Area of Science:

  • Neuroscience
  • Genetics
  • Molecular Biology

Background:

  • Familial Alzheimer's disease (AD) is linked to pathogenic variants in PSEN1 and PSEN2.
  • Sporadic AD shows differential regulation of PSEN2 3' untranslated region (3'UTR) isoforms, including short and extended forms.

Purpose of the Study:

  • To investigate the functional significance of PSEN2 3'UTR isoforms in Alzheimer's disease.
  • To establish in vitro models for assessing PSEN2 3'UTR isoform regulation.
  • To profile miRNA expression in AD and control brain samples.

Main Methods:

  • Developed in vitro models using HMC3 and SH-SY5Y cell lines with PSEN2 3'UTR constructs.
  • Performed small RNA sequencing on AD and control homogenate and synaptosome fractions.
  • Utilized BaseScope in-situ hybridization to analyze PSEN2 3'UTR isoform localization in human frontal cortex.

Main Results:

  • Short PSEN2 was predominantly cytoplasmic and decreased in AD frontal cortex; long PSEN2 was nuclear with similar levels in AD and controls.
  • Identified differentially regulated miRNAs in AD brain fractions, including miR-34c.
  • The long PSEN2 3'UTR contains binding sites for several differentially regulated miRNAs implicated in AD.

Conclusions:

  • Established an in vitro model for PSEN2 3'UTR isoform studies.
  • Characterized miRNA expression differences in human AD brain fractions.
  • Observed decreased PSEN2 transcript signal in human AD frontal cortex, highlighting the importance of 3'UTR isoform regulation in AD pathogenesis.