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A cGMP-applicable Expansion Method for Aggregates of Human Neural Stem and Progenitor Cells Derived From Pluripotent Stem Cells or Fetal Brain Tissue

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Low Levels of Amyloid Precursor Protein (APP) Promote Neurogenesis and Decrease Gliogenesis in Human Neural Stem

Raquel Coronel^1,2, Victoria López-Alonso³, Marta I Gallego⁴

¹Unidad de Regeneración Neural, Unidad Funcional de Investigación de Enfermedades Crónicas, Instituto de Salud Carlos III, 28220 Majadahonda, Madrid, Spain.

International Journal of Molecular Sciences

|October 14, 2023

Summary

Down-regulating amyloid precursor protein (APP) in human neural stem cells (hNSCs) promotes cell proliferation and neurogenesis. This finding contrasts with APP overexpression effects, offering new insights into APP

Keywords:

amyloid precursor protein cell fate specification gliogenesis human neural stem cells neurogenesis proliferation

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Published on: November 18, 2013

Area of Science:

Neuroscience
Cell Biology
Developmental Biology

Background:

Amyloid precursor protein (APP) is linked to Alzheimer's disease (AD), but its normal physiological roles remain unclear.
APP is a transmembrane glycoprotein highly expressed in the human central nervous system, particularly during brain development.
Previous studies showed APP overexpression in human neural stem cells (hNSCs) promotes gliogenesis and inhibits neurogenesis.

Purpose of the Study:

To investigate the cellular effects of down-regulating APP expression in hNSCs.
To determine the impact of APP silencing on cell death, proliferation, and cell fate.
To explore the role of beta-catenin in APP-mediated cellular effects.

Main Methods:

Utilized siRNA to silence APP expression in hNS1 cells, a model line for hNSCs.
Assessed cell death, proliferation, and differentiation (neurogenesis vs. gliogenesis).
Analyzed gene and protein expression levels of beta-catenin.

Main Results:

APP silencing resulted in increased cell proliferation in hNS1 cells.
Down-regulation of APP favored neurogenesis over gliogenesis.
Observed cellular effects were opposite to those seen with APP overexpression.

Conclusions:

APP expression levels intrinsically regulate hNSC proliferation and differentiation.
APP silencing promotes neurogenesis, suggesting a role in neural development.
Understanding APP's physiological functions is crucial for advancing AD research.