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Deregulation of neuronal miRNAs induced by amyloid-β or TAU pathology

Annerieke Sierksma1,2, Ashley Lu1,2, Evgenia Salta1,2

  • 1VIB Center for Brain & Disease Research, Leuven, Belgium.

Molecular Neurodegeneration
|October 14, 2018
PubMed
Abstract

Insights

Commonly upregulated microRNAs (miRNAs) were identified in Alzheimer's disease (AD) mouse models and patients. These specific miRNAs are linked to AD pathology but do not appear to cause cognitive decline in healthy mice.

Area of Science:

  • Neuroscience
  • Genetics
  • Molecular Biology

Background:

  • Alzheimer's disease (AD) is characterized by amyloid-β (Aβ) and TAU pathology, leading to episodic memory loss.
  • MicroRNA (miRNA) deregulation is observed in AD brains, but the causal relationship with Aβ/TAU pathology and cognitive decline remains unclear.

Purpose of the Study:

  • To investigate common miRNA expression changes in mouse models of AD with distinct pathologies (Aβ and TAU).
  • To determine if these altered miRNAs are present in human sporadic AD and if they contribute to cognitive deficits.

Main Methods:

  • miRNA sequencing (miRNAseq) was performed on cognitively intact and impaired APPtg and TAUtg mice and their wild-type littermates.
  • Differential gene expression analysis was conducted, with results validated by qPCR and in human AD brains.
  • Cellular expression was identified using fluorescent in situ hybridization, and functional annotation of predicted targets was performed.

Main Results:

  • Six miRNAs (miR-10a-5p, miR-142a-5p, miR-146a-5p, miR-155-5p, miR-211-5p, miR-455-5p) were commonly upregulated in both APPtg and TAUtg mice.
  • Four of these miRNAs (miR-142a-5p, miR-146a-5p, miR-155-5p, miR-455-5p) were also altered in human AD patients and are enriched in neurons.
  • Upregulating these miRNAs in wild-type mice did not induce AD-related cognitive disturbances.

Conclusions:

  • Divergent AD pathologies converge on common neuronal miRNA expression alterations.
  • Four specific miRNAs are implicated as part of a core pathological process in AD patients and mouse models.
  • These miRNAs may represent a protective response rather than a direct cause of cognitive decline in AD.
Keywords:
Alzheimer’s diseaseIn situ hybridizationmiR-mimicmiRNA-seqmicroRNA

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