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Updated: Jan 16, 2026

In Vitro Modeling of Down Syndrome Neurogenesis Using Human-Induced Pluripotent Stem Cells

In Vitro Modeling of Down Syndrome Neurogenesis Using Human-Induced Pluripotent Stem Cells

Published on: March 7, 2025

Trisomy 21 Disrupts Thyroid Hormones Signaling During Human iPSC-Derived Neural Differentiation In Vitro.

Janaina Sena de Souza¹, Sandra Sanchez-Sanchez¹, Nicolas Amelinez-Robles²

¹Department of Pediatrics, School of Medicine, University of California, San Diego, La Jolla, CA 90037, USA.

|September 26, 2025

Summary

Thyroid hormone signaling is altered in Down syndrome neural cells derived from stem cells. This imbalance impacts neurodevelopment and suggests potential therapeutic targets for cognitive deficits.

Keywords:

astrocytes deiodinase down syndrome gene expression iPSC neurons receptors thyroid hormones transporters

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A Guide to Generating and Using hiPSC Derived NPCs for the Study of Neurological Diseases

A Guide to Generating and Using hiPSC Derived NPCs for the Study of Neurological Diseases

Published on: February 21, 2015

Area of Science:

Neuroscience
Developmental Biology
Genetics

Background:

Thyroid hormones (THs) are crucial for brain development.
Dysregulation of THs is linked to cognitive deficits and neurodevelopmental disorders.
Down syndrome (DS), characterized by trisomy 21, often involves thyroid dysfunction and impaired neurogenesis.

Purpose of the Study:

To investigate THs signaling dynamics during neural differentiation in DS using human induced pluripotent stem cells (hiPSCs).
To analyze gene expression of THs regulators, transporters, receptors, and downstream targets in DS-derived neural cells.
To understand the cell-type-specific impact of THs dysregulation in DS neural development.

Main Methods:

Utilized hiPSCs from individuals with DS and controls.
Differentiated hiPSCs into neural progenitor cells (NPCs), astrocytes, and neurons.
Quantified gene expression of deiodinases (DIO2, DIO3), transporters (SLC16A10, SLC7A5), receptors (THRA, THRB), and neural genes (HOMER1, GRIN3A, GRIN3B) via RT-qPCR.
Performed multi-electrode array (MEA) recordings to assess neural activity.

Main Results:

DS-derived hiPSCs, NPCs, and neurons showed increased DIO2 and decreased DIO3 expression, with downregulated TH receptors.
DS-derived astrocytes displayed decreased DIO2, increased DIO3, altered transporter expression (SLC16A10, SLC7A5), and reduced TH receptors.
DS-derived neurons exhibited downregulated neural genes (HOMER1, GRIN3A, GRIN3B) and impaired spontaneous electrical activity.

Conclusions:

DS hiPSC-derived neural cells exhibit a cell-type-specific imbalance in THs availability and signaling.
This THs dysregulation provides mechanistic insight into neural cell function in DS.
Identified potential therapeutic targets for addressing THs-related contributions to DS neurodevelopmental outcomes.