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The Effect of a Novel Mica Nanoparticle, STB-MP, on an Alzheimer's Disease Patient-Induced PSC-Derived Cortical Brain Organoid Model.


ABSTRACT: Alzheimer's disease (AD) is one of the most well-known neurodegenerative diseases, with a substantial amount of advancements in the field of neuroscience and AD. Despite such progress, there has been no significant improvement in AD treatments. To improve in developing a research platform for AD treatment, AD patient-derived induced pluripotent stem cell (iPSC) was employed to generate cortical brain organoids, expressing AD phenotypes, with the accumulation of amyloid-beta (Aβ) and hyperphosphorylated tau (pTau). We have investigated the use of a medical grade mica nanoparticle, STB-MP, as a treatment to decrease the expression of AD's major hallmarks. STB-MP treatment did not inhibit the expression of pTau; however, accumulated Aβ plaques were diminished in STB-MP treated AD organoids. STB-MP seemed to activate the autophagy pathway, by mTOR inhibition, and also decreased γ-secretase activity by decreasing pro-inflammatory cytokine levels. To sum up, the development of AD brain organoids successfully mimics AD phenotype expressions, and thus it could be used as a screening platform for novel AD treatment assessments.

SUBMITTER: Kim NG 

PROVIDER: S-EPMC10005775 | biostudies-literature | 2023 Feb

REPOSITORIES: biostudies-literature

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The Effect of a Novel Mica Nanoparticle, STB-MP, on an Alzheimer's Disease Patient-Induced PSC-Derived Cortical Brain Organoid Model.

Kim Nam Gyo NG   Jung Dong Ju DJ   Jung Yeon-Kwon YK   Kang Kyung-Sun KS  

Nanomaterials (Basel, Switzerland) 20230227 5


Alzheimer's disease (AD) is one of the most well-known neurodegenerative diseases, with a substantial amount of advancements in the field of neuroscience and AD. Despite such progress, there has been no significant improvement in AD treatments. To improve in developing a research platform for AD treatment, AD patient-derived induced pluripotent stem cell (iPSC) was employed to generate cortical brain organoids, expressing AD phenotypes, with the accumulation of amyloid-beta (Aβ) and hyperphospho  ...[more]

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