Aging-relevant human basal forebrain cholinergic neurons as a cell model for Alzheimer’s disease
Molecular Neurodegeneration, ISSN: 1750-1326, Vol: 15, Issue: 1, Page: 61
2020
- 16Citations
- 29Captures
- 1Mentions
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- Citations16
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- 16
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- Captures29
- Readers29
- 29
- Mentions1
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Aging-relevant human basal forebrain cholinergic neurons as a cell model for Alzheimer's disease.
Mol Neurodegener. 2020 Oct 21;15(1):61. Authors: Ma S, Zang T, Liu ML, Zhang CL PubMed: 33087140 Submit Comment
Article Description
Background: Alzheimer’s disease (AD) is an adult-onset mental disorder with aging as a major risk factor. Early and progressive degeneration of basal forebrain cholinergic neurons (BFCNs) contributes substantially to cognitive impairments of AD. An aging-relevant cell model of BFCNs will critically help understand AD and identify potential therapeutics. Recent studies demonstrate that induced neurons directly reprogrammed from adult human skin fibroblasts retain aging-associated features. However, human induced BFCNs (hiBFCNs) have yet to be achieved. Methods: We examined a reprogramming procedure for the generation of aging-relevant hiBFCNs through virus-mediated expression of fate-determining transcription factors. Skin fibroblasts were obtained from healthy young persons, healthy adults and sporadic AD patients. Properties of the induced neurons were examined by immunocytochemistry, qRT-PCR, western blotting, and electrophysiology. Results: We established a protocol for efficient generation of hiBFCNs from adult human skin fibroblasts. They show electrophysiological properties of mature neurons and express BFCN-specific markers, such as CHAT, p75NTR, ISL1, and VACHT. As a proof-of-concept, our preliminary results further reveal that hiBFCNs from sporadic AD patients exhibit time-dependent TAU hyperphosphorylation in the soma and dysfunctional nucleocytoplasmic transport activities. Conclusions: Aging-relevant BFCNs can be directly reprogrammed from human skin fibroblasts of healthy adults and sporadic AD patients. They show promises as an aging-relevant cell model for understanding AD pathology and may be employed for therapeutics identification for AD.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85093099255&origin=inward; http://dx.doi.org/10.1186/s13024-020-00411-6; http://www.ncbi.nlm.nih.gov/pubmed/33087140; https://molecularneurodegeneration.biomedcentral.com/articles/10.1186/s13024-020-00411-6; https://dx.doi.org/10.1186/s13024-020-00411-6
Springer Science and Business Media LLC
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