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Basic Science and Pathogenesis.

Debomoy K Lahiri1,2, Ruizhi Wang2, Bryan Maloney2

  • 1Indiana Alzheimer's Disease Research Center, Indianapolis, IN, USA.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 23, 2025
PubMed
Summary
This summary is machine-generated.

MicroRNA-153-3p may serve as a therapeutic target for Alzheimer's disease (AD) and related dementias (ADRDs). This microRNA (miRNA) reduces key proteins implicated in neurodegeneration, suggesting biomarker potential.

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Area of Science:

  • Neuroscience
  • Genetics
  • Molecular Biology

Background:

  • Alzheimer's disease (AD) and related dementias (ADRDs) are common neurodegenerative disorders with unknown triggers.
  • MicroRNAs (miRNAs) are crucial in regulating biological and pathological processes in neurodegeneration.
  • Key pathological hallmarks include amyloid plaques (amyloid-β peptides from APP), neurofibrillary tangles (tau proteins), and alpha-synuclein (SNCA) in synucleinopathies.

Purpose of the Study:

  • To investigate the role of miR-153-3p in Alzheimer's disease (AD) risk.
  • To determine miR-153-3p's function in regulating critical neurodegenerative proteins like amyloid precursor protein (APP), alpha-synuclein (SNCA), and Repressor Element 1-Silencing Transcription factor (REST).

Main Methods:

  • Quantitative real-time PCR (qRT-PCR) to measure miR-153 levels in brain tissues from non-cognitively impaired (NCI) and AD subjects.
  • Association studies of miR-153-3p and its single nucleotide polymorphisms (SNPs) with AD risk and endophenotypes using autopsy brain tissues and ADNI participant genotyping.
  • In vitro studies using induced pluripotent stem cell (iPSC)-derived neuronal cells and human cell lines to elucidate the mechanism of miR-153-3p action.

Main Results:

  • Elevated miR-153-3p levels correlated with a reduced probability of AD.
  • Increased REST levels were associated with a higher likelihood of AD.
  • miR-153-3p significantly reduced the activity and protein levels of REST, APP, and SNCA.
  • miR-153-3p influenced REST expression and neuronal differentiation in iPSC-derived neuronal stem cells.
  • RNA sequencing, proteomics, and interactome analysis indicated miR-153-3p's involvement in axonal guidance.

Conclusions:

  • miR-153-3p acts as a master regulator, decreasing key neurodegeneration-related proteins (APP, SNCA, REST).
  • These findings highlight miR-153-3p's potential as a therapeutic target and biomarker for Alzheimer's disease (AD) and related dementias (ADRDs).
  • Future research will include profiling miR-153 in early-onset AD cases.