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Review
. 2021 Aug 2;10(8):740.
doi: 10.3390/biology10080740.

Brain Organoids: Filling the Need for a Human Model of Neurological Disorder

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Review

Brain Organoids: Filling the Need for a Human Model of Neurological Disorder

Philip Jalink et al. Biology (Basel). .

Abstract

Neurological disorders are among the leading causes of death worldwide, accounting for almost all onsets of dementia in the elderly, and are known to negatively affect motor ability, mental and cognitive performance, as well as overall wellbeing and happiness. Currently, most neurological disorders go untreated due to a lack of viable treatment options. The reason for this lack of options is s poor understanding of the disorders, primarily due to research models that do not translate well into the human in vivo system. Current models for researching neurological disorders, neurodevelopment, and drug interactions in the central nervous system include in vitro monolayer cell cultures, and in vivo animal models. These models have shortcomings when it comes to translating research about disorder pathology, development, and treatment to humans. Brain organoids are three-dimensional (3D) cultures of stem cell-derived neural cells that mimic the development of the in vivo human brain with high degrees of accuracy. Researchers have started developing these miniature brains to model neurodevelopment, and neuropathology. Brain organoids have been used to model a wide range of neurological disorders, including the complex and poorly understood neurodevelopmental and neurodegenerative disorders. In this review, we discuss the brain organoid technology, placing special focus on the different brain organoid models that have been developed, discussing their strengths, weaknesses, and uses in neurological disease modeling.

Keywords: 3D culture; disease modeling; neurodevelopment; stem cells; tissue morphogenesis.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
A schematic overview of the creation of and uses for organoid models of neurological disorders. Overview of the different research outcome measures and tools available to researchers working with brain organoids.
Figure 2
Figure 2
Schematic overview of the differentiation progress of organoids with patterning factors. Outcome differences between the use of high or low concentrations of patterning factors and the spatiotemporal control of patterning.
Figure 3
Figure 3
Non-exhaustive schematic overview of the different types of cells found in different organoid models.

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References

    1. Thakur K.T., Albanese E., Giannakopoulos P., Jette N., Linde M., Prince M.J., Steiner T.J., Dua T. Disease Control Priorities: Mental, Neurological, and Substance Use Disorders. 3rd ed. Volume 4. The World Bank; Washington, DC, USA: 2016. Neurological Disorders; pp. 87–107.
    1. Smoller J.W., Kendler K., Craddock N., Lee P.H., Neale B.M., Nurnberger J.N., Ripke S., Santangelo S., Sullivan P.S., Neale B.N., et al. Identification of risk loci with shared effects on five major psychiatric disorders: A genome-wide analysis. Lancet. 2013;381:1371–1379. - PMC - PubMed
    1. Lee S.H., Ripke S., Neale B.M., Faraone S.V., Purcell S.M., Perlis R.H., Mowry B.J., Thapar A., Goddard M.E., Witte J.S., et al. Genetic relationship between five psychiatric disorders estimated from genome-wide SNPs. Nat. Genet. 2013;45:984–994. - PMC - PubMed
    1. Bulik-Sullivan B., Finucane H.K., Anttila V., Gusev A., Day F.R., Loh P.R., Duncan L., Perry J.R.B., Patterson N., Robinson E.B., et al. An atlas of genetic correlations across human diseases and traits. Nat. Genet. 2015;47:1236–1241. doi: 10.1038/ng.3406. - DOI - PMC - PubMed
    1. Cannon J.R., Greenamyre J.T. The role of environmental exposures in neurodegeneration and neurodegenerative diseases. Toxicol. Sci. 2011;124:225–250. doi: 10.1093/toxsci/kfr239. - DOI - PMC - PubMed

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