ANKRD1 sustains a neurogenic BMSC niche and counters cognitive aging

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Authors: Zifei Wang, Xiaoyun Liu, Wenyu Zhen, Fei Xu, Rui Wang, Wenhu Fan, Wenhao Zhang, Yulong Zhang, Wansu Sun, Mingyue Wu, Jiacai He, Hao Gu
+1 more Hengguo Zhang
Cited by: 1
References: 75

Abstract

Craniomaxillofacial bone marrow mesenchymal stromal cells (BMSCs) retaining neural crest-derived neurogenic niche is driven by lineage memory and niche homeostasis. Elucidating how the neurogenic potential is maintained is critical for neurological health. Here, we explored a neural crest-like progenitor niche in BMSCs with high neurogenic and proliferative capacity by single-cell transcriptomics. In which, ANKRD1 is a pivotal regulator sustaining the neurogenic reservoir. Importantly, ANKRD1 expression in this niche declines with aging and lineage commitment, coinciding with its redistribution from a diffuse nucleoplasmic pattern to perinuclear enrichment along the nuclear lamina and loss of neural potential. Mechanistically, ANKRD1 preserves neurogenic capacity by directly binding super-enhancers of neural marker genes (SOX2, NESTIN) and maintaining open chromatin architecture. Critically, neuron-targeted ANKRD1 delivery rescues spatial memory deficits in aged mice. These findings establish ANKRD1 as a therapeutically tractable regulator that sustains neurogenic chromatin reservoirs to support neurocognitive resilience, opening avenues to counter cognitive aging.

Fields of Study & Subjects

Neurogenesis and neuroplasticity mechanisms Phosphodiesterase function and regulation Alzheimer's disease research and treatments

Publication details

Journal / source
International Journal of Oral Science
Publisher
Springer Science and Business Media LLC
Volume
18
Issue
1
Publication date
1 March 2026
Language
EN