MAPT-A152T mutation drives neuronal hyperactivity through Fyn-NMDAR signaling in human iPSC-Derived neurons: Insights into Alzheimer's pathogenesis
These data demonstrate that the A152T mutation in the <i>MAPT</i> gene increases neuronal excitability through the tau-Fyn-NMDAR pathway in excitatory neurons, shedding light on its role in AD pathogenesis.
Authors
- Setsu Endoh‐Yamagami (ORCID: https://orcid.org/0000-0002-7574-750X)
- Hideyuki Okano (ORCID: https://orcid.org/0000-0001-7482-5935)
- Hiroko Bannai (ORCID: https://orcid.org/0000-0002-0951-488X)
- Hirokazu Tanabe
- Koichi Saito (ORCID: https://orcid.org/0000-0001-6497-5286)
- Takashi Sasaki (ORCID: https://orcid.org/0000-0002-6275-046X)
- Etsuko Sano
- Kazuhiko Nakata
- Sumihiro Maeda (ORCID: https://orcid.org/0000-0002-0701-6860)
- M Itsuno
- C Oyama
Institutions
- Waseda University (JP)
- Fujifilm (Japan) (JP)
- Keio University Hospital (JP)
- Keihin (Japan) (JP)
Publication Details
- Journal
- Regenerative Therapy
- Published
- 2024-12-24
- DOI
- https://doi.org/10.1016/j.reth.2024.12.009
- Citations
- 2
- Primary Topic
- Alzheimer's disease research and treatments
- Type
- article
- Field-Weighted Citation Impact
- 0.65
Funders
- Japan Agency for Medical Research and Development
- Japan Science and Technology Corporation
- Keio University
- Fujifilm Corporation
- Japan Society for the Promotion of Science