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A C

B

Figure 3. Application of organoids in glioblastoma. (A) The neoCOR model utilizes CRISPR/Cas9 technology to introduce oncogenic mutations,
effectively simulating brain tumorigenesis. Reproduced with permission Copyright © 2018 Cell Press. (B) In vitro therapeutic evaluation of GBOs
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revealed differential responses to radiation, temozolomide, gefitinib, trametinib, and everolimus, with significant reductions in Ki67+ cells and gene set
enrichments indicative of treatment efficacy, as determined by confocal imaging, quantitative analysis, and genetic pathway targeting. Reproduced with
permission. Copyright © 2020 Elsevier Inc. (C) Transcriptome profiling of GPDCs for unveiling glioma subtypes and predicting patient prognosis
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through differential expression and prognostic signature analysis. Reproduced with permission. Copyright © 2021 Elsevier B.V.
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Abbreviations: GBO: Glioblastoma organoids; GPDCs: Glioma patient-derived tumor cells; neoCOR: Neoplastic cerebral organoid.
stages are closely associated with the loss of dopaminergic of patients with PD, exacerbating motor disabilities and
neuronal axons, and as the disease progresses, axonal cognitive decline. 124
degeneration and the death of dopaminergic neurons
occur. In addition to the impairment of dopaminergic In PD, the activation of various cell death pathways
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neurons in the substantia nigra, alterations in the is involved, including increased calcium ion influx,
serotonergic pathways of the locus coeruleus and the raphe enhanced oxidative stress, mitochondrial and lysosomal
nuclei are also considered key factors in the development dysfunction, dysregulation of microglial autophagy-
of PD. Furthermore, the disruption of the cholinergic lysosomal function, and imbalances in sphingolipid
pathway can also affect the motor and cognitive functions metabolism. 125-127 Specifically, α-synuclein oligomers alter

Volume 1 Issue 1 (2025) 10 doi: 10.36922/or.8261