Early pathogenic event of Alzheimer’s disease documented in iPSCs from patients with PSEN1 mutations | Zendy

Juan Yang | Zendy; Hanzhi Zhao | Zendy; Yu Ma | Zendy; Guilai Shi | Zendy; Jian Song | Zendy; Yu Tang | Zendy; Song Li | Zendy; Ting Li | Zendy; Nan Liu | Zendy; Fan Tang | Zendy; Junjie Gu | Zendy; Lingling Zhang | Zendy; Zhuohua Zhang | Zendy; Xiao Hui Zhang | Zendy; Ying Jin | Zendy; Weidong Le | Zendy

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Early pathogenic event of Alzheimer’s disease documented in iPSCs from patients with PSEN1 mutations

Author(s) -

Juan Yang,

Hanzhi Zhao,

Yu Ma,

Guilai Shi,

Jian Song,

Yu Tang,

Song Li,

Ting Li,

Nan Liu,

Fan Tang,

Junjie Gu,

Lingling Zhang,

Zhuohua Zhang,

Xiao Hui Zhang,

Ying Jin,

Weidong Le

Publication year - 2016

Publication title -

oncotarget

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.373

H-Index - 127

ISSN - 1949-2553

DOI - 10.18632/oncotarget.13776

Subject(s) - induced pluripotent stem cell , psen1 , neuroscience , neurogenesis , somatic cell , wnt signaling pathway , biology , neural stem cell , medicine , pathogenesis , progenitor cell , stem cell , disease , alzheimer's disease , embryonic stem cell , microbiology and biotechnology , pathology , presenilin , genetics , signal transduction , gene

Alzheimer's disease (AD) is the most common age-related dementia characterized by progressive neuronal loss. However, the molecular mechanisms for the neuronal loss is still debated. Here, we used induced pluripotent stem cells (iPSCs) derived from somatic cells of familial AD patients carrying PSEN1 mutations to study the early pathogenic event of AD. We found that premature neuronal differentiation with decreased proliferation and increased apoptosis occured in AD-iPSC-derived neural progenitor cells (AD-NPCs) once neuronal differentiation was initiated, together with higher levels of Aβ42 and phosphorylated tau. Premature neuronal differentiation in AD-NPCs was caused by PSEN1 mutations and might be correlated to multiple dysregulated processes including but not limited to Wnt-Notch pathway. Our study documented previously unappreciated early NPC dysfunction in AD-NPCs, providing valuable new insights into the early mechanisms underlying AD pathogenesis.

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