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EPS and iPS Cells in Disease Research

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Embryonic and induced pluripotent stem cells are excellent models for disease research because of their ability to self-renew and differentiate into most cell types. Somatic cells from a patient are isolated and reprogrammed into induced pluripotent stem cells or iPSCs. These iPSCs are later differentiated into the desired cell type, which mirrors the diseased cell of the patient. In this way, disease models have been created for investigating diseases such as Down syndrome, type I diabetes,...

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

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Human stem cell-based models to study synaptic dysfunction and cognition in schizophrenia: A narrative review.

Stephanie Santarriaga¹, Kaia Gerlovin², Yasmine Layadi³

¹Center for Genomic Medicine, Massachusetts General Hospital, Boston, MA, USA; Chemical Biology and Therapeutic Science Program, Broad Institute of MIT and Harvard, Cambridge, MA, USA; Department of Psychiatry, Harvard Medical School, Boston, MA, USA.

Schizophrenia Research

|March 16, 2023

Summary

Schizophrenia cognitive deficits stem from synaptic dysfunction. Patient-derived stem cells offer a new way to study synaptic plasticity and develop targeted treatments for improved learning and memory.

Keywords:

Cognitive deficits Schizophrenia Synaptic plasticity iPSCs

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Area of Science:

Neuroscience
Psychiatry
Stem Cell Biology

Background:

Cognitive impairment significantly impacts functional outcomes in schizophrenia.
Synaptic dysfunction is a leading hypothesis for the cognitive deficits observed in schizophrenia.
Current therapeutic strategies struggle to effectively target synaptic plasticity and cognitive deficits.

Purpose of the Study:

To elucidate the role of synaptic plasticity in cognitive function.
To review evidence linking synaptic dysfunction to schizophrenia.
To explore patient-derived induced-pluripotent stem cells (iPSCs) as a model for studying synaptic plasticity in vitro.

Main Methods:

Review of existing literature on synaptic plasticity and schizophrenia.
In vitro studies utilizing patient-derived iPSCs.
Analysis of molecular mechanisms underlying learning and memory in disease contexts.

Main Results:

Synaptic plasticity is crucial for cognitive processes.
Substantial evidence supports synaptic dysfunction as a core feature of schizophrenia.
Patient-derived iPSCs provide a viable platform for investigating synaptic plasticity relevant to schizophrenia.

Conclusions:

Understanding synaptic plasticity in schizophrenia is key to developing novel therapeutics.
Patient-derived iPSCs represent a promising translational tool.
Future research should bridge basic science with clinical applications for treatment prediction and development.